Serum Galectin-3 Levels Research Articles

Serum galectin-3 levels in patients with psoriasis.

Galectin-3 is a β-galactoside-binding lectin associated with cellular proliferation, inflammation and angiogenesis, which are the major characteristics of psoriatic skin. To investigate serum galectin-3 levels in psoriasis patients compared with healthy controls and to study its relationship with disease characteristics. Seventy-eight patients diagnosed with psoriasis and 78 age- and sex-matched healthy volunteers were included in the study. Serum galectin-3, IL-17, IL-6 and TNF-α levels were measured using Enzyme-linked immunosorbent assay (ELISA). Serum Galectin-3, IL-17, IL-6 and TNF-α levels were significantly higher in psoriasis patients compared with control group (P<.001, P=.003, P<.001 and P<.001, respectively). A cut-off value of 10ng/mL for galectin-3 was set after receiver operating characteristic analysis. A serum galectin-3 level >10ng/mL increased the risk of psoriasis by 14.5 times (95% CI: 6.6-32.3, P<.001) and a serum galectin-3 level >10ng/mL predicted psoriasis with 83.3% sensitivity and 74.3% specificity. No statistically significant association was observed between serum galectin-3 concentrations and disease characteristics including disease severity, presence of psoriatic arthritis, nail involvement and psoriatic comorbidity. No statistically significant correlation was observed between serum galectin-3 level and serum IL-17, IL-6 and TNF-α levels (all three P values>.05). Elevated serum galectin-3 levels in psoriasis patients may indicate a possible role of galectin-3 in pathogenesis of psoriasis.

Role of stimulating growth factor 2 and galectin-3 in predicting the ventricular tachyarrhythmias in patients with ischemic cardiomyopathy

Aim. To assess the role of stimulating growth factor 2 (ST-2) and galectin-3 in predicting the ventricular tachyarrhythmias (VTA) in patients with coronary artery disease (CAD) and left ventricular ejection fraction (LVEF) &lt;35%.Material and methods. The study included 40 patients (men, 36 (90,0%); median age, 64,5 [57,5; 68,5] years) with CAD, NYHA class IIIII heart failure, LVEF &lt;35%, indications for implantable cardioverter defibrillator (ICD) (primary prevention of sudden cardiac death). Prior to ICD implantation, patients were measured for serum ST-2 and galectin-3 levels. For 18 months, patients were assessed for arrhythmic events recorded in the ICD memory.Results. The 1st group consisted of 10 (25,0%) patients who had VTA episodes, arrested by antitachycardia pacing or shock during 18-month follow-up. The 2nd group consisted of 30 (75,0%) patients without VTA episodes. It was found that ST-2 concentration &gt;22,48 ng/ml (p=0,02) and galectin-3 &gt;10,95 ng/ml (p=0,009) corresponded to appropriate ICD discharge. Multivariate ROC analysis demonstrated that the only independent predictor of VTA was ST-2 elevation (odds ratio, 1,11; 95% CI, 1,01-1,21; p=0,023).Conclusion. An increase in the concentration of both ST-2 &gt;22,48 ng/ml and galectin-3 &gt;10,95 ng/ml had a high predictive value in assessing the VTA risk in patients with ischemic cardiomyopathy. In multivariate analysis, an increase in ST-2 &gt;22,48 ng/ml was an independent predictor of VTA.

Genetic variants in LGALS3 are related to lower galectin-3 serum levels and clinical outcomes in systemic sclerosis patients: A case-control study

Introduction Systemic sclerosis (SSc) is a rare complex disease characterized by vascular damage, autoimmunity, and extensive skin and internal organs fibrosis. Galectin-3 (Gal-3) is encoded by gene LGALS3 (Lectin, Galactoside-Binding, Soluble, 3; 14q22.3) and it has been reported to play a central role in self-tolerance, inflammation, and fibrosis. Objective To investigate associations among LGALS3 single nucleotide polymorphisms (SNPs) and serum levels Gal-3 and SSc susceptibility and their clinical features. Methods A case-control study with 88 patients and 151 matched controls was performed. LGALS3 variants were analyzed by the TaqMan real-time polymerase chain reaction (PCR) system whereas Gal-3 serum levels were measured by sandwich enzyme linked immunosorbent assay (ELISA). Associations among genotypes, clinical features, and Gal-3 levels were performed by univariable and multivariable analysis through statistical packages. Results The LGALS3 rs4652 A/C genotype was more frequent in SSc patients than controls according to overdominant model [OR 1.89 (CI 95% 1.01 − 3.52); p = .046]. Also, LGALS3 rs4652 C/C polymorphic genotype was associated with lower patient Gal-3 levels (p = .03) and control group (p = 0.005), as noted by generalized linear model (GLM). The LGALS3 rs1009977 G/T controls showed higher Gal-3 levels than wild-type and polymorphic genotypes (p = .03); however, in SSc patients, no difference was found. None of the LGALS3 SNPs or Gal-3 levels was associated with clinical manifestations in SSc patients. Considering only the SSc group, GLM analysis pointed LGALS3 rs4652 and rs2075601, pulmonary arterial hypertension (PAH), myopathy, and health assessment questionnaire (HAQ) and scleroderma health assessment questionnaire (SHAQ) as important predictors for Gal-3 levels. Conclusion The LGALS3 rs4652 A/C was more frequent in SSc patients and related to lower Gal-3 levels. These findings were corroborated through a GLM to estimate Gal-3 values. Also, by model equations, Gal-3 levels may be predicted by HAQ, SHAQ, PAH, myopathy, and LGALS3 rs4652 and rs2075601 factors. In these ways, we suggest that galectins may be promising biomarkers to identify susceptibility to SSc as well as to identify HAQ, SHAQ, PAH, and myopathy outcomes.

Evaluation of the relationship between serum and urine galectin-3 levels and microalbuminuria in patients with Type 2 Diabetes Mellitus

Amaç: Bu çalışmanın amacı Tip 2 diyabetes mellitusu olan hastalarda mikroalbuminüri gelişimi ile serum ve idrar galektin-3 düzeyleri arasındaki ilişkiyi değerlendirmektir. Yöntem: Tip 2 diyabet tanısı olan mikroalbüminüri gelişmiş 30 hasta ve tip 2 diyabet tanısı olan normoalbüminürik 30 hasta çalışmaya dahil edildi. Tüm hastalarda açlık kan şekeri, hemoglobin A1c, kan üre nitrojeni, kreatinin, düşük dansiteli lipoprotein kolesterol, total kolesterol, tam idrar tetkiki, spot idrarda albümin, spot idrarda kreatinin, serum galektin-3 ve idrar galektin-3 çalışıldı. Serum galektin-3, idrar galektin-3, hemoglobin A1c, düşük dansiteli lipoprotein kolesterol, total kolesterol mikroalbüminürik ve normoalbüminürik gruplar arasında karşılaştırıldı. Bulgular: Çalışmamızda mikroalbüminürik grupta, normoalbüminürik gruba göre hem serum galektin-3 düzeyi (20.1±14.9 ng/ml ve 4.8±5.6 ng/ml, p &amp;lt;0.001) hem de idrar galektin-3 düzeyi (19.6±18.7 ng/ml ve 10.5±10.2 ng/ml, p=0.027) yüksek tespit edildi. Mikroalbüminüri düzeyi ile serum ve idrar galektin-3 düzeyi arasında pozitif korelasyon tespit edildi (r=0.614, p&amp;lt;0.01 ve r=0.268, p&amp;lt;0.05, sırasıyla). Serum galektin-3 düzeyinin, mikroalbüminüriyi öngörmede bağımsız bir etken olduğu görüldü (Odds oranı:1.26, güven aralığı:1.07-1.46, p=0.004). Sonuç: Tip 2 diyabetes mellitusu olan hastalarda mikroalbüminürisi olan hastalarda normoalbüminürisi olanlara göre hem serum hem de idrar galektin-3 düzeylerinde artış saptandı. Çalışmamızın bulguları diyabetik nefropatide galektin-3’ün bir biyobelirteç olarak kullanılabileceği görüşünü desteklemiştir.

The role of galectin-3 and its genetic variants in tumor risk and survival of patients with surgically resected early-stage non-small cell lung cancer.

Background The aim of this study was to investigate the possible relationship between galectin-3 gene variants, serum level, gene expression level, and the risks and survivals of resectable non-small cell lung cancer patients. Methods The rs4644 and rs4652 variants of galectin-3 were genotyped by TaqMan single nucleotide polymorphism assay using genomic deoxyribonucleic acid isolated from the peripheral blood of 65 (54 males, 11 females; mean age: 60.1±11.9 years; range, 34 to 83 years) with Stage IA-IIIA non-small cell lung cancer who underwent primary surgical treatment and 95 healthy individuals (48 males, 47 females; mean age: 53.9±13.5 years; range, 32 to 87 years) between March 2017 and September 2018. Circulating galectin-3 levels in serum samples of the patient and control groups were assessed by enzyme-linked immunosorbent assay. Messenger ribonucleic acid expression of galectin-3 in tumor and surrounding tissues of the patient group was examined by real-time quantitative polymerase chain reaction. Both predictive and prognostic significance of the results were analyzed. Results The presence of angiolymphatic invasion was significant in the patients with rs4652 AA genotype (p=0.04). Serum galectin-3 levels were significantly higher in the patients than the controls (p<0.0001). The patients with rs4644 CA/CC (p<0.0001 and p<0.0001) and rs4652 AA/AC (p=0.001 and p<0.0001) genotypes had higher serum galectin-3 levels than their corresponding controls. Serum galectin-3 levels increased in the presence of vascular invasion in patients with both rs4644 AC (p=0.03) and rs4652 AC (p=0.019) genotypes. The receiver operating characteristic curve suggested serum galectin-3 level as a strong predictive marker for the patient group with a cut-off value of 17.089 ng/mL (area under the curve: 0.910±0.04; 95% confidence interval: 0.832-0.988; p<0.001). Univariate analysis revealed the association of lower serum galectin-3 levels with better survival (p=0.048). Multivariate survival analysis showed that only high serum galectin-3 levels tended to be related to survival of the patients (hazard ratio: 5.106; 95% confidence interval: 0.956-27.267; p=0.056). Conclusion The presence of galectin-3 gene variants may lead to histopathological differences among patients with non-small cell lung cancer. Serum galectin-3 level may be a valuable diagnostic biomarker and be associated with survival of these patients.

Association of Serum Galectin-3 Level with Albuminuria and Renal Function in Type 2 Diabetic Iraqi Patients

Background: Galectin-3 is a category of ?- galactoside binding Lectin. It has been involved in renalinflammation and fibrosis. We examined the relationship between galectin-3 level and nephropathy in T2DMpatients with or without microalbuminuria in comparison healthy controls.Methods: Ninety T2DM patients they were graded as (3 groups) depending on (ACR) albumin to creatininevalue: normalbuminuria (ACR &lt; 30 mg / g), micro albuminuria (ACR 30-300 mg / g); and macroalbuminuria(ACR &gt; 300 mg / g). In addition, 30 healthy control subject. The serum galectin-3 was determined by anenzyme-linked immune sorbent assay (ELISA) for 90 T2DM patients and 30 healthy subjects. And alsobiochemical parameters measured included FBG, HbA1c, urea, creatinine, and uric acid.Result: Serum galectin-3 was significantly raised in T2DM patients with macroalbuminuria in comparing tohealthy group and also to other patients groups (p&lt;0.001). Galectin-3 level was positively related with eachof ACR, FBS, HbA1c, urea, creatinine. whilst, eGFR was negatively correlated with galectin-3Conclusion: Galectin-3 level is essentially higher with T2DM at all stages of DN, particularly inmacroalbuminuria patients.

Galectin-3: a new biomarker for differentiating periodic fever, adenitis, pharyngitis, aphthous stomatitis (PFAPA) syndrome from familial Mediterranean fever?

Differentiating PFAPA (periodic fever, aphthosis, pharyngitis, and adenitis) syndrome from familial Mediterranean fever (FMF) could be challenging in some cases. Galectin-3 is a lectin with regulatory functions in apoptosis and inflammation. We aimed to test whether galectin-3 could be a biomarker for differentiating PFAPA syndrome from FMF. Patients with PFAPA syndrome, FMF, cryopyrin-associated periodic syndrome (CAPS), and streptococcal pharyngitis, and healthy controls were included in this study. Serum galectin-3 levels were measured using enzyme-linked immunosorbent assay. Eighty-seven patients (36 with PFAPA, 39 with FMF, 8 with CAPS, 4 with streptococcal pharyngitis), and 17 healthy controls were included. Blood samples were drawn during attacks from 20 PFAPA and 7 FMF patients and attack-free periods from 22 PFAPA, 35 FMF, and 8 CAPS patients. The median serum galectin-3 level in the PFAPA-attack group (1.025ng/ml) was significantly lower than the levels in healthy control (2.367ng/ml), streptococcal pharyngitis (3.021ng/ml), FMF attack (2.402ng/ml), and FMF-attack-free groups (2.797ng/ml) (p = 0.006, 0.03, 0.01, and < 0.001, respectively). PFAPA-attack-free group had lower galectin-3 levels than the FMF-attack-free group (1.794 vs. 2.797ng/ml, respectively; p = 0.01). Galectin-3 levels did not differ significantly between CAPS and attack-free PFAPA patients (1.439ng/ml vs. 1.794ng/ml, respectively; p = 0.63). In our study, for the first time, we defined galectin-3 as a promising biomarker that differs between PFAPA and FMF patients during both disease flares and attack-free periods. Further studies with high number of patients could validate its role as a biomarker.

Myocardial extracellular volume quantification by computed tomography predicts outcomes in patients with severe aortic stenosis.

The extent of myocardial fibrosis in patients with severe aortic stenosis might have an important prognostic value. Non-invasive imaging to quantify myocardial fibrosis by measuring extracellular volume fraction might have an important clinical utility prior to aortic valve intervention. Seventy-five consecutive patients with severe aortic stenosis, and 19 normal subjects were prospectively recruited and underwent pre- and post-contrast computed tomography for estimating myocardial extracellular volume fraction. Serum level of galectin-3 was measured and 2-dimensional echocardiography was performed to characterize the extent of cardiac damage using a recently published aortic stenosis staging classification. Extracellular volume fraction was higher in patients with aortic stenosis compared to normal subjects (40.0±11% vs. 21.6±5.6%; respectively, p<0.001). In patients with aortic stenosis, extracellular volume fraction correlated with markers of left ventricular decompensation including New York Heart Association functional class, left atrial volume, staging classification of aortic stenosis and lower left ventricular ejection fraction. Out of 75 patients in the AS group, 49 underwent TAVI, 6 surgical AVR, 2 balloon valvuloplasty, and 18 did not undergo any type of intervention. At 12-months after aortic valve intervention, extracellular volume fraction predicted the combined outcomes of stroke and hospitalization for heart failure with an area under the curve of 0.77 (95% confidence interval: 0.65-0.88). A trend for correlation between serum galectin-3 and extracellular volume was noted. In patients with severe aortic stenosis undergoing computed tomography before aortic valve intervention, quantification of extracellular volume fraction correlated with functional status and markers of left ventricular decompensation, and predicted the 12-months composite adverse clinical outcomes. Implementation of this novel technique might aid in the risk stratification process before aortic valve interventions.

Elevated levels of soluble ST2 but not galectin-3 are associated with increased risk of mortality in hemodialysis patients.

BackgroundThe soluble forms of suppression of tumorigenicity-2 (ST2) and galectin-3 have been proposed as novel biomarkers for cardiac fibrosis and heart failure, as well as predictors of cardiovascular events and mortality. However, there are limited data on the association between soluble ST2 and galectin-3 and clinical outcomes in patients with kidney failure on replacement therapy. To determine this, we examined the associations between soluble ST2 and galectin-3 and all-cause mortality and cardiovascular events in patients on hemodialysis.MethodsThis study included maintenance hemodialysis patients (over 18 years old) who consented to preserve their serum in the Biobank at our institution between March 2014 and March 2015. We used Cox proportional hazards regression analysis to evaluate the associations between soluble ST2, galectin-3 levels, and clinical outcomes. The primary outcome was all-cause mortality, the secondary outcome was cardiovascular disease, and patients were followed for both outcomes until March 2018.ResultsA total of 296 patients were analyzed in this study. The mean age was 57 ± 13 years, and 53.0% were male. Serum concentration of soluble ST2 was significantly associated with higher mortality, after adjustment for confounding factors, but was not associated with cardiovascular disease. Serum galectin-3 level was not independently associated with either outcome after adjustment.ConclusionElevated soluble ST2 is independently associated with an increased risk of mortality, but not with cardiovascular disease, in patients on hemodialysis. Elevated galectin-3 was not associated with mortality or cardiovascular disease.

The serum galectin-3 levels are associated with the severity and prognosis of ischemic stroke.

Galectin-3, a microglia/macrophage-derived inflammatory mediator, plays a role in the stroke progression. In this single-center prospective study, we included 288 consecutive patients with a first-ever acute ischemic stroke to assess the association between galectin-3 serum level and clinical severity at admission and outcome at discharge by univariate and multivariate logistic regression. The results were presented as odds ratios (OR) and 95% confidence intervals (CI). Patients with high severity and poor outcomes had higher serum levels of galectin-3 (P<0.001 and P<0.001). Multivariate analysis suggested that a galectin-3 serum level in the highest quartile (The lowest three quartiles[Q1-3] as the reference) was associated with poor functional outcome (OR, 3.15; 95% CI, 2.44–3.87). The AUC (standard error) for the NIHSS and the combined model were 0.764 (0.031) and 0.823 (0.027), corresponding to a difference of 0.059 (0.004). This study shows that higher serum levels of galectin-3 are associated with stroke severity at admission and stroke prognosis at discharge in ischemic stroke.

Analysis of galectin-3 levels as a source of coronary heart disease risk during periodontitis.

Different evidence has shown that Galectins have a key role as modulators of cell surface functions and signaling in a wide range of inflammatory diseases during their preclinical stages. The aim of this study was to analyze the association and impact of periodontitis and coronary heart disease (CHD) on salivary and serum Galectin-3 in patients with periodontitis and CHD. For the present study, healthy controls (n=38), periodontitis (n=40), CHD (n=39), and a combination of periodontitis +CHD (n=38) patients were enrolled and analyzed. In each patient, demographic characteristics and a full-mouth clinical periodontal examination were achieved. Moreover, serum and salivary samples were collected to assess Galectin-3 and Endothelin-1 (ET-1) levels. The Jonckheere-Terpstra p-trend and Spearman's correlation tests as well as uni- and linear regression analyses were used to analyze the study data. Patients with periodontitis (serum, p=.003; saliva, p<.001) and periodontitis + CHD groups (serum p=.004; saliva, p<.001) had higher median serum and salivary concentrations of Galectin-3 in comparison with CHD and healthy controls. Serum (p=.006) and salivary (p=.009) Galectin-3 levels were significantly correlated with serum ET-1. The multivariate regression analysis highlighted that periodontitis (p=.047) was the significant predictor of serum Galectin-3 levels while ET-1 (p=.028) was the significant predictor of salivary Galectin-3 levels. The results showed that patients with periodontitis and periodontitis + CHD presented significant higher serum and salivary Galectin-3 levels in comparison with CHD patients and healthy subjects. Periodontitis and ET-1 were the significant predictors of serum and salivary Galectin-3 levels, respectively.

Circulating biomarkers of cardiac fibrosis: do they correlate with the echocardiographic parameters of the myocardial mechanics in systemic sclerosis?

Abstract Funding Acknowledgements Type of funding sources: None. Background In systemic sclerosis (SSc) myocardial fibrosis contributes to the impairment of the myocardial function resulting in manifest diastolic and subclinical systolic dysfunction of the left ventricle (LV) and impaired left atrial (LA) function. The pathophysiology of this connective tissue disease is still not fully elucidated. Recently, however, elevated serum levels of galectin-3 and soluble suppression of tumorigenicity 2 (sST2) have been reported in SSc patients suggesting that these fibrotic markers may participate in the fibrotic process in this disease. Thus we aimed to investigate the potential associations between galectin-3 and sST2 levels and the echocardiographic markers of the LV and LA function in SSc patients. Methods Forty patients (57.3 ± 13.7 years, 36 female) were enrolled into the study. In addition to the conventional echocardiography, tissue Doppler and speckle-tracking-derived strain techniques were used to estimate the LV systolic and diastolic function as well as the LA size and function. To assess the correlations between galectin-3 and sST2 levels and the echocardiographic variables, partial correlation method was used with age as correcting factor. Results In age adjusted analysis galectin-3 level showed significant correlation with LV global longitudinal strain (r = 0.460, p = 0.005); grade of LV diastolic dysfunction (r = 0.394, p = 0.013); septal e’ (r=-0.369, p = 0.021); septal E/e’ (r = 0.380, p = 0.017) and with the grade of mitral regurgitation (r = 0.323, p = 0.048) (Figure 1). No significant correlation was found between sST2 levels and the echocardiographic variables. Conclusions Galectin-3 levels, but not sST2 levels show significant correlation with the parameters of the LV diastolic function and with LV global longitudinal strain, a parameter reflecting the subclinical impairment of the LV systolic function. Galectin-3 may be a useful biomarker for identifying SSc patients with high risk for cardiac involvement. Abstract Figure 1

Serum Galectin-3 as a Potential Predictive Biomarker Is Associated with Poststroke Cognitive Impairment.

Objective Galectin-3, an inflammatory mediator derived from microglia, participates in the pathophysiological process of various neurological diseases. However, the relationship between galectin-3 and poststroke cognitive impairment (PSCI) remains ambiguous. This research purposed to prove whether serum galectin-3 can predict PSCI. Methods In the end, an aggregate of 416 patients with the first acute ischemic stroke (AIS) were continuously and prospectively enrolled in the study. Upon admission, the baseline data of AIS patients were collected, and their serum galectin-3 levels were measured. Three months after the stroke, the Montreal Cognitive Scale (MoCA) was utilized to measure the cognitive function of AIS patients, and PSCI was defined as a MoCA score less than 26 points. Results Premised on the MoCA scores, patients were categorized into PSCI cohort and non-PSCI cohort. The two AIS patient cohorts did not exhibit any statistical difference in their baseline characteristics (p > 0.05). However, the serum galectin-3 level of AIS patients in the PSCI cohort was considerably elevated (p < 0.001). Pearson correlation analysis illustrated that serum galectin-3 level was negatively linked to MoCA score (r = −0.396, p < 0.05). The findings from the receiver-operating curve (ROC) illustrated that the sensitivity of serum galectin-3 as a possible biomarker for diagnosing PSCI was 66%, and the specificity was 94%. The cut-off value of serum galectin-3 to diagnose PSCI is 6.3 ng/mL (OR = 5.49, p < 0.001). Upon controlling for different variables, serum galectin-3 level remained to be an independent predictor of PSCI (p < 0.001). Conclusions Elevated serum galectin-3 levels are linked to a higher risk of PSCI. Serum galectin-3 could be a prospective biomarker for predicting PSCI.

Galectin-3 is not useful for hepatocellular carcinoma surveillance in cirrhotic patients but it may be a marker of cirrhosis development.

Aim of the studyUltrasound surveillance for hepatocellular carcinoma (HCC) among cirrhotic patients is the currently used modality but it is operator dependent. Combining a tumor marker with ultrasound may improve sensitivity for early HCC detection. Our aim was to assess the galectin-3 level among HCC and cirrhotic patients on top of chronic hepatitis C to evaluate its possible role as a tumor marker for HCC surveillance among cirrhotic patients.Material and methodsThe study was conducted on 160 subjects. They were grouped as follows: group 1: 40 patients with HCC secondary to liver cirrhosis on top of chronic hepatitis C; group 2: 40 patients with cirrhosis secondary to chronic hepatitis C; group 3: 40 patients with chronic hepatitis C without advanced fibrosis; group 4: 40 healthy controls. Serum galectin-3 levels were determined in all subjects using ELISA.ResultsSerum galectin-3 level was significantly higher in HCC patients than in those with chronic hepatitis C (p < 0.001). Also it was significantly higher among cirrhotic patients than in patients with chronic hepatitis C (p < 0.001). But on comparing HCC patients with cirrhotic patients, serum galectin-3 levels were not significantly different (p = 0.926).Conclusions: Galectin-3 levels cannot be used as an additional method for surveillance of HCC among cirrhotic patients.

Effect of galectin-3 in the pathogenesis of arteriovenous fistula stenosis formation

Objective This study sought to investigate the effect of local expression of galectin-3 in the development of stenotic arteriovenous fistula (AVF). Methods We collected stenotic venous tissues, adjacent nonstenotic venous tissues, and blood samples from end-stage renal disease (ESRD) patients with AVF stenosis, while normal venous tissues and blood samples were collected from ESRD patients before AVF creation as controls. Also blood samples were collected from ESRD patients with nonstenosis functional AVF. Galectin-3, proliferating cell nuclear antigen (PCNA), matrix metalloproteinase-9 (MMP-9), and α-SMA expression in the venous tissues were examined by immunohistochemistry, and the ERK1/2 pathway activity in the intima was accessed by western blot. Serum galectin-3 level was measured by ELISA. Thereafter, human pulmonary arterial smooth muscle cells (HPASMCs) were cultured in vitro, and the interaction between Galectin-3 and ERK1/2 pathway in HPASMCs was estimated by western blot. Results ESRD patients with stenotic AVF had a significant higher serum galectin-3 level than normal controls, and patients with non-stenotic functional AVF. The expression levels of galectin-3, phosphorylated ERK1/2, PCNA, MMP-9, and α-SMA in the stenotic venous tissues were higher than that in the normal venous tissues or the adjacent nonstenotic AVF venous tissues. Correlation analysis showed that the expression of galectin-3 of the neointima was positively correlated with PCNA and α-SMA in the stenotic AVF venous tissues. In HPASMCs, galectin-3 can increase the activity of phosphorylated ERK1/2 and promote the expression of α-SMA. Conclusion In the stenotic AVF of ESRD patients, expression of the galectin-3 was significantly increased, showing a positive relation with neointima development.

The association between serum galectin-3 level and its placental production in patients with preeclampsia.

Galectin-3 is β-galactoside-binding lectin, used in cardiology as a biomarker of heart failure. Available research suggest galectin-3 may play a role in the development of preeclampsia. Seventy seven women were included in the study: 39 with preeclampsia and 38 with uncomplicated pregnancy. Patients underwent blood sample analysis (galectin-3, N-terminal pro-brain natriuretic peptide (NT-proBNP), soluble fms-like tyrosine kinase-1 (sFlt-1), placental growth factor (PlGF), cystatin C, creatinine) and echocardiographic examination. After delivery, placental tissue samples were obtained for immunohistochemistry evaluation. In patients with preeclampsia, serum galectin-3 levels (11.8 versus 9.5 ng/ml; p = 0.004) and galectin-3 expression in placental tissue (immunoreactive score (IRS) in extravillous trophoblasts: 9 versus 5; p = 0.002; in syncytiotrophoblasts: 6 versus 2, p < 0.001) were significantly higher than in the control group. Serum NT-proBNP and sFlt-1 levels, sFlt-1/PlGF ratio, serum creatinine and cystatin C levels were significantly higher, whereas serum PlGF levels and estimated glomerular filtration rate (eGFR) were significantly lower in preeclamptic patients than in uncomplicated pregnancy. On echocardiography, preeclamptic women had significantly greater thickness of interventricular septum (IVS) and left ventricle posterior wall (PW) and significantly worse left ventricle diastolic function (higher E/e' values). Serum galectin-3 level did not correlate with any other biochemical parameters, as well as the vast majority of echocardiographic parameters. Significant correlation between serum galectin-3 and its placental expression in syncytiotrophoblasts (STB) was revealed. Renal function parameters and NT-proBNP correlated with antiangiogenic state. This study demonstrated increased serum galectin-3 levels and placental galectin-3 production in preeclamptic patients, in comparison to women with uncomplicated pregnancy. Myocardial dysfunction and worse renal function parameters in patients with preeclampsia were not related to galectin-3. The main source of galectin-3 in maternal blood was its placental production. In the development of preeclampsia, galectin-3 may act as a compensatory mechanism to impaired placentation in early pregnancy.

Evaluation of galectins 1 and 3 expression in canine melanoma

ABSTRACT: Canine melanoma is a frequently-occuring neoplasm in dogs and presents as malignant and highly metastatic in this context, studies that contribute to the understanding of the tumor microenvironment in melanoma include the role of galectins. Galectins are proteins of the family of animal lectins that display carbohydrate recognition domains. Galectin-1 and galectin-3 are associated with neoplastic transformation, neoplastic cell survival, angiogenesis, immune system evasion, and metastasis. The goal of this study was to establish a correlation between expression patterns of galectin-1 and galectin-3 and the different degrees of aggressiveness of canine melanoma, as well as to determine serum concentration of galectin-3 in dogs with melanoma. Galectin-1 and galectin-3 expression was analyzed by immunohistochemistry in 30 canine melanomas, six melanocytomas and nine metastatic lymph nodes from patients whose primary tumors were also processed and analyzed. Serum samples from 30 dogs were collected and galectin-3 concentration was determined by ELISA and compared to the samples of 10 healthy dogs. Canine melanoma samples expressed galectin-1 in the cytoplasm and presented a variable pattern of galectin-3 staining depending on melanoma aggressiveness. We observed a decrease in the percentage of cells with cytoplasmic galectin-3 immunolabeling simultaneous to the increased nuclear staining intensity, while there was also a decrease in the percent frequency of nuclear galectin-3 immunolabeled cells according to progression of melanoma, comparing the least to the most aggressive cases. Dogs with melanoma had increased serum levels of galectin-3 when compared to healthy animals, suggesting its potential biomarker of patients with melanoma.

Value of Galectin-3 assay in children with heart failure secondary to congenital heart diseases: a prospective study

BackgroundGalectin-3 is a new biomarker, which plays an important role in tissue inflammation, cardiac remodeling, and fibrosis. It can be readily measured in the circulation to detect early heart failure (HF). This study aimed to assess the value of galectin-3 assay in early diagnosis of children with heart failure secondary to congenital heart disease (CHD) and correlate it with the patients’ outcome.MethodsThis prospective cohort study included 75 children diagnosed to have CHD; {Group A: 45 CHD children with HF symptoms and reduced ejection fraction (REF) and Group B: 30 CHD children with no HF symptoms and normal ejection fraction (NEF)}. They were compared to 40 age- and sex-matched controls (Group C). Children with CHD undergone history taking, Ross HF classification, Echocardiographic assessment and laboratory investigations including serum galactin-3 level.ResultsGalectin-3 serum level increased in CHD children, and it showed significant increase in (Gp A) compared to Gp B or Gp C (p = ≤ 0.001). In addition, serum level of Galactin-3 was correlated positively with Ross classification (r = 0.68, p = 0.018) and negatively correlated to EF% (r= -0.61, p ≤ 0.001). Galactin-3 showed better diagnostic value than Ross HF classification in early diagnosis of HF in CHD children with a cut point (≥ 10.4), significantly had 96.7% sensitivity, 90% specificity, 91% positive predictive value, 93.2% negative predictive value, with area under the curve (AUC = 0.96) and 93% accuracy. While there was a significant correlation between Ross HF classification and HF outcome in (Gp A) children (p = 0.05), we did not find any significant correlation between serum galectin-3 level and HF mortality in same group (p = 0.08).ConclusionsGalectin-3 assay is a promising marker for early diagnosis of HF in children with CHD; but it has no role in detecting HF mortality.

Relevant correlation of Galectin-3 with a novel morphological classification system for LAA closure – the end of echocardiographic follow up after occluder implantation?

Abstract Introduction Echocardiographic detection of residual peri-device leakage (PDL) after percutaneous left atrial appendage closure (LAAC) remains crucial. Significance of PDL and cardiac tissue remodeling after LAAC are still poorly understood but might have diagnostic implications. This study aims to characterize and verify if a novel echocardiographic classification system to asses the success of LAAC in combination with quantifiable biomarkers of cardiovascular tissue remodeling can help in the prediction of PDL. Methods Patients eligible for LAAC were included. Serum levels of the cardiac remodeling marker Galectin-3 were determined before device implantation (baseline), 45 days (45d) and 6 months (6M) after LAAC using ELISAs. Transesophageal echocardiography (TEE) was carried out to assess success of the LAAC procedure. All echo images were retrospectively evaluated by two independent investigators. Based on the amount of echodensity and luceny inside the devices after LAAC, three types can be distinguished that grade the degree of closure of the LAA. Type A has complete homogenous echodensity in 0, 45, 90 and 135°, indicating completely thrombosed device. Type B shows inhomogeneous echo-lucencies (&amp;lt;50% of device). Type C describes a partially thrombosed device with echo-lucencies &amp;gt;50%. Novel classification according to Hamadanchi, Jena, Germany (Fig. 1). Results We included 44 patients (characteristics listed in Table 1). Complete LAAC (without any residual flow) was achieved in 64% (28 patients) after 45 days and in 80% (35 patients) after 6 months. Mean PDL diameter was 3.5±1.5mm. Type A showed the lowest rate of PDL after 45d (Type A: 22% vs. Type B: 33% vs. Type C: 88%; p=0.007) and after 6M (Type A: 12% vs. Type B: 28% vs. Type C: 100%; p=0.002). Galectin-3 levels did not show a relevant difference regarding the type of AF at baseline (paroxysmal AF: 11.7±5.4 ng/ml vs. permanent AF: 12.1±6.3 ng/ml; p=0.45). We observed a significant increase and distribution of serum levels of Galectin-3 [ng/ml] after 45 days among the three types (Baseline: 13.1±5.8; 45d: 16.3±7.2 (Type A) vs. 19.2±8.6 (Type B) vs. 25.8±9.4 (Type C); p=0.031) followed after 6 months by a drop of Galectin-3 for type A and B toward and below baseline levels (6M: 8.9±3.1 (Type A) vs. 12.4±5.5 (Type B)) whereas type C persisted in showing elevated Galectin-3 levels compared to all other types (6M: 17.5±4.5 (Type C); p&amp;lt;0.001), Fig. 2. Correlation analysis shows a significant negative correlation trend between Galectin-3 and mean PDL diameter (−0.51; p=0.016) after 45 days and a relevant positive correlation after 6 months (0.58; p=0.017). Conclusion After LAAC, Galectin-3 levels are elevated, as a marker of myocardial fibrosis in the LAA. Depending on the degree of closure of the LAA, Galectin-3 decreases to the baseline level or stays elevated in case of relevant PDL and could therefore be considered as a new biomarker for closure success. Funding Acknowledgement Type of funding source: None

Dynamics of Galectin-3 serum levels after percutaneous occlusion of the left atrial appendage: a new surrogate parameter for successful LAA closure?

Abstract Introduction Left atrial cardiac tissue remodeling following left atrial appendage closure (LAAC) is a scientifically neglected phenomenon until now but might have impact on functional outcome of patients suffering from atrial fibrillation (AF). Thus, our study is focused on quantification of key biomarkers reflecting fibrosis development as a major component within cardiovascular tissue remodeling. Methods Patients (CHA2DS2VASC score ≥1, HASBLED score ≥3) with bleeding complications under anticoagulation therapy and therefore eligible for LAAC were included in the present study. Serum levels of biomarkers of cardiac fibrosis and remodeling (Galectin-3, ST2/IL-2, ST2/IL-1, B domain containing Tenascin-C (B+ Tn-C), C domain containing Tenascin- C (C+ Tn-C)) were determined before device implantation (baseline), 45 days (45d) and 6 months (6M) after LAAC using commercially available ELISAs. To quantify functional outcome, all patients performed a 6-minutes walk test (6- MWT). Transesophageal echocardiography (TEE) was carried out to assess success of the LAAC procedure regarding peri-device leakage (PDL). Results We included 33 patients (age: 73.5±6.7 years; 21 men (64%) and 12 women (36%); BMI: 29.1±5.1 kg/m2; CHA2DS2VASC score: 4.2±1.2; left ventricular ejection fraction: 61.1±9.3%; mean occluder size: 25.9±3.9 mm; type of AF: 46% paroxysmal (15 patients), 55% permanent (18 patients)). Complete LAAC (without any residual low) was achieved in 60% (19 patients) after 45 days and in 87% (29 patients) after 6 months. At baseline, Galectin-3 levels did not show a relevant difference regarding the type of AF (paroxysmal AF: 14.7±5.4 ng/ml vs. permanent AF: 13.1±6.3 ng/ml; p=0.45). We observed a significant increase of serum levels of Galectin-3 [ng/ml] after 45 days vs. baseline (baseline: 13.3±5.8 vs. 45d: 18.3±10.6; p=0.005) with a return to baseline levels after 6 months (baseline: 13.3±5.8 vs. 6M: 12.5±5.4; p=0.28). Compared to patients with successful LAAC, patients with PDL had a trend towards higher levels of Galectin-3 after 6 months (11.3±5.5 ng/ml vs. 16.1±4.1 ng/ml, p=0.09). Measurements of other fibrosis markers were statistically not significantly different. The walking distance measured by the 6-MWT increased significantly from 298.5±89.5 meters at baseline to 335.5±95.1 meters (p=0.04) after 45d and remained significantly elevated after 6M (346.7±122.7 meters; p=0.02). Conclusion The implantation of an LAA occluder device is accompanied by significantly increased circulating levels of the fibrosis biomarker Galectin-3 after 45 days in patients with AF. The regression in serum levels after 6 months probably reflects a successful fibrotic remodeling in the left atrial appendage over time and might be used as surrogate parameter for LAAC success. Increased and stable exercise tolerance after 45 days can be observed. Funding Acknowledgement Type of funding source: None