Galectin-3 Research Articles

TP53 gene and myeloid neoplasms

TP53 gene, an important tumor suppressor gene, has been a hot topic in tumor molecular biology. The assessment of TP53 mutations/deletions is becoming a routine clinical practice for chronic lymphocytic leukemia patients. In recent years, a number of studies have shown that TP53 mutations/deletions in myeloid neoplasms also suggests poor prognosis. Myeloid neoplasms patients with TP53 mutations/deletions show a good response to hypomethylation agents such as decitabine and azacitidine, and some novel experimental drugs targeting TP53 mutations/deletions, such as galectin inhibitor GCS-100 and BH3 mimetics are also being studied. To further understand prognostic significance of TP53 mutations/deletions in myeloid neoplasms and elaborate its potential as novel therapy target, this article reviews literatures on the relationship between TP53 mutations/deletion and prognosis of myeloid neoplasms, related molecular mechanisms and treatment progress. Key words: Genes, p53; Prognosis; Myeloid neoplasms

870P - Expression of Galectin-1 Determines Tumor Recurrence and Cancer-specific Survival in Patients with pT3 Upper Urinary Tract Urothelial Carcinoma

Background: Upper urinary tract urothelial carcinoma (UTUC) is an aggressive and lethal disease. For patients with locally advanced UTUC, recurrence of tumor is frequent, and lacks of predictive biologic markers limited the choice of postoperative treatment. Galectin-1 (GAL1) is a β-galactoside-binding protein, participating in many parts of tumorigenesis, including cell proliferation, invasiveness, metastasis, and angiogenesis. However, the role of GAL1 in UTUC has not been fully investigated. The aim of this study was to examine the prognostic impact of GAL1 in patients with UTUC. Methods: The study enrolled 86 UTUC patients who underwent radical nephroureterectomy and bladder cuff excision with final pathologically diagnosed as pT3N0 stage between January 2005 and December 2012. Perioperative characteristics and pathologic features were recorded. Immunohistochemical staining of tumor specimens using anti-GAL1 antibody were performed. UTUC cell line (BFTC-909) was used for in vitro study of tumor invasiveness and migration. Kaplan-Meier analyses and Cox proportional regression models were used for univariate and multivariate survival analyses. Results: Using 10% expression of GAL1 protein as a cuff-off point, the study population could be classified as GAL1-high (GAL1 > 10%, n = 35) or GAL1-low (GAL1 ≤ 10%; n = 51) group. Basic clinicopathologic characteristics were comparable between two groups. In univariate analysis, high GAL1 expression was significantly associated with a worse recurrence-free survival (RFS; p = 0.028) and cancer-specific survival (CSS; p = 0.025). Multivariate analysis showed GAL1-high is an independent factor for RFS (HR 2.43; 95% CI 1.17-5.05, p = 0.018) and CSS (HR 4.04; 95% CI 1.25-13.03, p = 0.019). In vitro study, we found that knockdown of GAL1 reduced UTUC cancer cell migration and invasion significantly. Conclusions: Galectin-1 expression is a reliable prognostic factor for locally advanced UTUC. GAL1 inhibition may serve as a potential therapeutic target for patients with UTUC. Legal entity responsible for the study: Yu-Li Su Funding: None Disclosure: All authors have declared no conflicts of interest.

Arterial stiffness, aldosterone and galectin-3 in patients with metabolic syndrome without heart failure

Aim: Carotid-femoral pulse wave velocity (cfPWV) is a method of evaluating arterial stiffness that is associated with increased risk of cardiovascular complications. Galectin-3 (GAL3) and aldosterone (ALDO) are profibrogenic substances. Study objectives were to evaluate GAL3 and ALDO in patients with metabolic syndrome (MetS) without HF and to identify their relationship with arterial stiffness.

Fatty-binding protein and galectin of Baylisascaris schroederi: Prokaryotic expression and preliminary evaluation of serodiagnostic potential.

Baylisascaris schroederi is a common parasite of captive giant pandas. The diagnosis of this ascariasis is normally carried out by a sedimentation-floatation method or PCR to detect eggs in feces, but neither method is suitable for early diagnosis. Fatty acid-binding protein (FABP) and galectin (GAL) exist in various animals and participate in important biology of parasites. Because of their good immunogenicity, they are seen as potential antigens for the diagnosis of parasitic diseases. In this study, we cloned and expressed recombinant FABP and GAL from B. schroederi (rBs-FABP and rBs-GAL) and developed indirect enzyme-linked immunosorbent assays (ELISAs) to evaluate their potential for diagnosing ascariasis in giant pandas. Immunolocalization showed that Bs-FABP and Bs-GAL were widely distributed in adult worms. The ELISA based on rBs-FABP showed sensitivity of 95.8% (23/24) and specificity of 100% (12/12), and that based on rBs-GAL had sensitivity of 91.7% (22/24) and specificity of 100% (12/12).

X-ray structure of a protease-resistant mutant form of human galectin-9 having two carbohydrate recognition domains with a metal-binding site

Galectin-9 (G9) is a tandem-repeat type β-galactoside-specific animal lectin having N-terminal and C-terminal carbohydrate recognition domains (N-CRD and C-CRD, respectively) joined by a linker peptide that is involved in the immune system. G9 is divalent in glycan binding, and structural information about the spatial arrangement of the two CRDs is very important for elucidating its biological functions. As G9 is protease sensitive due to the long linker, the protease-resistant mutant form of G9 (G9Null) was developed by modification of the linker peptide, while retaining its biological functions. The X-ray structure of a mutant form of G9Null with the replacement of Arg221 by Ser (G9Null_R221S) having two CRDs was determined. The structure of G9Null_R221S was compact to associate the two CRDs in the back-to-back orientation with a large interface area, including hydrogen bonds and hydrophobic interactions. A metal ion was newly found in the galectin structure, possibly contributing to the stable structure of protein. The presented X-ray structure was thought to be one of the stable structures of G9, which likely occurs in solution. This was supported by structural comparisons with other tandem-repeated galectins and the analyses of protein thermostability by CD spectra measurements.

Galectin-3 correlates with arrhythmogenic right ventricular cardiomyopathy and predicts the risk of ventricular ­arrhythmias in patients with implantable defibrillators

Background Arrhythmogenic right ventricular dysplasia (ARVD) is a heritable disorder characterized by fibro-fatty replacement of right ventricular myocytes, increased risk of ventricular arrhythmias, and sudden cardiac death. Galectin-3 (GAL3) is known to play an important role in a number of fibrotic conditions, including cardiac fibrosis. Many studies have focused on the association between GAL3 levels and cardiac fibrosis in heart failure. However, the role of GAL3 in the pathogenesis of ARVD and ventricular arrhythmias has not yet been evaluated thoroughly. The aim of this study was to explore GAL3 levels in patients with ARVD and its association with ventricular arrhythmias.Methods Twenty-nine patients with ARVD and 24 controls were included. All patients with ARVD had an implantable cardiac defibrillator (ICD) for primary or secondary prevention. Ventricular arrhythmia history was obtained from a chart review and ICD data interrogation. Galectin-3 levels were measured using an enzyme-linked immunosorbent assay.Results Patients with ARVD had higher plasma GAL3 levels (16.9 ± 2.6 ng/mL vs 11.3 ± 1.8 ng/mL, P < 0.001) than the control group. Ten patients had sustained or non-sustained ventricular arrhythmias during follow-up. In the multivariable analysis, left ventricular disease involvement (HR: 1.05; 95% CI: [1.01-1.12]; P = 0.03); functional capacity >2 (HR: 1.21; 95% CI: [1.13-1.31]; P < 0.005); and GAL3 levels (HR: 1.05; 95% CI: [1.00-1.11]; P = 0.01) independently predicted VT/VF.Conclusion We demonstrated that serum GAL3 was significantly elevated in patients with ARVD. Also, serum GAL 3 levels could be regarded as a candidate biomarker in the diagnosis of ARVD which needs to be tested in larger prospective studies. In addition, GAL3 levels were higher in patients with VT/VF as compared with those without VT/VF.

Abstract LB-282: Two different strategies of delivery CRISPR/Cas9 system to gene edit rs4644 SNP in LGALS3 gene

Abstract Galectin-3 is a glycoprotein of 31KDa with a chimeric structure. It is encoded by a single gene, LGALS3, located on chromosome 14. Previous studies showed a relation between the single nucleotide polymorphism (SNP) (rs4644, c.191C&amp;gt;A, p.Pro64His) and the risk of cancer. In literature, some data show different results indicating that SNP could have different roles in base on the tissues. The aim of our study is to create isogenic cell lines that differ only for SNP permitting further studies about the function of SNP in different cancers. The “generation” of the cell lines is performed with a Clustered Regularly Interspaced Short Palindromic Repeats-associated Endonuclease 9 (CRISPR/Cas9) system. We have used two different strategies to deliver the system. In the first strategy, our aim was the reduction of the problem of efficiency of transfection that could depend on different cell lines. In fact, we have used the lentivirus method to deliver all components of the CRISPR/Cas9 on Nthy-Ori (normal thyroid tissue) and HCT 116 +/+ (colorectal cancer tissue) cells. Two different vectors (pCW-Cas9 and pLXgRNA) are used to build up the inducible CRISPR/Cas9 system and HR410PA-1 vector (transfected by Lipofectamine 3000) is used to knock-in. HR410PA-1 is a particular vector that facilities the homologous recombination (HR) to repair the double strand break. Moreover, to improve HR, we use also Scr7, which is an inhibitor of DNA IV ligase. In the second approach, we have used the double nickase system using two modified Cas9 vectors (SpCas9D10a) that produce only a single strand break. In this way, the problem of off-targets is notably reduced. In this approach, the knock-in is due to or single-stranded oligodeoxynucleotides (ssODNs) or HR410PA-1 vector. The first results show that some of the transfected cells are edited in a correct way. In the further steps, we will isolate the “positive clones” using the selection cassette in HR410PA-1 vector (GFP protein and/or puromycin) or the single cell dilution assay (1 cell/well) for the transfected cells with ssODNs. Citation Format: Alda Corrado, Irene Lepori, Simona Miglietta, Simone Batoni, Marianna Vitiello, Monica Evangelista, Elisa Chisci, Roberto Giovannoni, Laura Poliseno, Federica Gemignani, Stefano Landi. Two different strategies of delivery CRISPR/Cas9 system to gene edit rs4644 SNP in LGALS3 gene [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr LB-282. doi:10.1158/1538-7445.AM2017-LB-282

Phytochemical remedies: a key strategy towards reversing the aggressive murine colon cancer

Colon cancer accounts for about 500,000 death cases worldwide annually and represents approximately 6.5% of cancers in Egypt. This study employed a murine colon cancer model to identify the mechanism of the therapeutic value of gallic acid or ellagic acid against colon carcinogenesis in vivo. Fifty adult male rats were distributed into five groups. Group (1) was set as a negative control group. Groups (2), (3), (4), and (5) were intrarectally injected with N-methylnitrosourea to induce colon cancer. Group (2) was kept untreated, whereas group (3) and (4) were orally administered gallic acid and ellagic acid, respectively. Group (5) received intraperitoneal injection of 5-fluorouracil. The administration of gallic acid, ellagic acid or 5-fluorouracil harmonized the hazardous effect of N-methylnitrosourea in colon cancer-afflicted rats. This was evidenced by the significant depletion in both of serum tumor associated glycoprotein-72 (TAG72) and galectin-3 (GAL3) levels as well as the significant downregulation in the expression level of frizzled-8 receptor (FRZ-8) gene and significant amplification of adenomatous polyposis coli gene expression level in the colon tissues of all treated groups. Intriguingly, such treatments resulted in a notable improvement in the pathological features of colon tissue sections of N-methylnitrosourea-challenged rats. Generally speaking, the current investigation emphasizes the favorable impact of gallic acid and ellagic acid in monitoring the progression of colon cancer in vivo. We suggest that the mitigation of Wnt signaling pathway may be the probable mechanism by which these compounds can offer their therapeutic actions against colon cancer.

Hepatic fibrosis scores and serum biomarkers in pediatric hepatology.

Hepatic fibrosis scores and serum biomarkers in pediatric hepatology.

Combined inhibition of autophagy protein 5 and galectin-1 by thiodigalactoside reduces diet-induced obesity through induction of white fat browning.

Our previous study demonstrated that thiodigalactoside (TDG) ameliorates obesity by targeted inhibition of galectin-1 (GAL1). Here, for the first time, we report the unexpected role of GAL1 and ATG5 inhibition by TDG in lipid metabolism. Core thermogenic marker proteins and genes were highly induced in white adipose tissue (WAT) of rats fed a high fat diet (HFD) and TDG, resulting in the significant development of brown fat-like adipocytes in inguinal WAT. TDG treatment reduced weight gain and fat mass as well as activated brown adipose tissue (BAT) in HFD-fed rats. TDG also reduced protein levels of LC3-II and increased protein levels of P62, suggesting its possible role in suppression of autophagy. Combined inhibition of GAL1 and ATG5 by TDG treatment protected rats against both HFD-induced adipogenesis as well as lipogenesis, as evidenced by suppression of CCAAT/enhancer-binding protein alpha, peroxisome proliferator-activated receptor gamma and fatty acid synthase. In conclusion, the present findings suggest that TDG plays a role in browning and lipid catabolism by combined inhibition of GAL1 and ATG5 and thus may have potential therapeutic implications in the regulation of energy homeostasis via its action in WAT. © 2017 IUBMB Life, 69(7):510-521, 2017.

Association Between LGALS3 Gene Polymorphisms and Survival in Non–Small Cell Lung Cancer Patients Treated With Definitive Radiation Therapy

Association Between LGALS3 Gene Polymorphisms and Survival in Non–Small Cell Lung Cancer Patients Treated With Definitive Radiation Therapy

The Human Lectin Galectin‐3 Recognizes Chondroitin Sulfate Proteoglycans (CSPGs) and Sulfated Glycosaminoglycans

Glycan‐binding proteins are classified in two major but distinct groups: lectins and glycosaminoglycan (GAG)‐binding proteins (GAGBPs). The multifunctional human lectin galectin‐3 (Gal‐3) is a member of the first group. GAGBPs, on the other hand, include a variety of non‐lectin proteins such as growth factors, cytokines, morphogens and ECM (extracellular matrix) proteins. The general structures of the binding sites of lectins, their preferred glycan structures and their mode of action are fundamentally different from those of GAGBPs. A member of one group rarely possesses the characteristics of both groups. Our data, however, show that Gal‐3 is a notable exception to that rule. In the present study, we report several significant findings. First, calorimetric and spectroscopic data show for the first time that Gal‐3 behaves like a GAGBP. The lectin interacts with unmodified sulfated GAGs (heparin and chondroitin sulfates) and chondroitin sulfate proteoglycans (CSPGs) at physiological pH and NaCl concentration. Second, the binding of sulfated GAGs and CSPGs to Gal‐3 is not a result of non‐specific interactions, rather sulfated GAGs and CSPGs specifically bind to Gal‐3, apparently, via the LacNAc/lactose binding site of Gal‐3. Finally, while heparin and chondroitin sulfate B (dermatan sulfate) are found to be monovalent ligands of Gal‐3, chondroitin sulfate A (CSA), chondroitin sulfate C (CSC) and bovine CSPG engage in multivalent binding with Gal‐3. Such multivalent binding leads to the formation of noncovalent cross‐linked complexes, which is reversible by lactose and different sulfated GAGs. Hill plot analysis of calorimetric data show that the binding of CSA, CSC and bovine CSPG to Gal‐3 is associated with progressive negative cooperativity effects. The present study provides a foundation for discovering new functions of GAGs and CSPGs mediated by Gal‐3 [1].Support or Funding InformationNational Science FoundationMichigan Technological University

OTX008 inhibits retinal neovascularization in oxygen-induced retinopathy mice

Objective To investigate the inhibitory effects and possible related mechanism of OTX008 [a selective inhibitor of galectin-1 (Galectin-1)] on retinal neovascularization (RNV) in mouse model of oxygen-induced retinopathy (OIR). Methods 7-day-old (P7) C57BL/6J mice were randomly (according to random number table) divided into 4 groups including normal group, OIR group, OIR-OTX008 group and OIR-phosphate buffered saline (PBS) group. To establish the OIR mouse model, mice from all groups except normal group were expose to (75±2)% oxygen for 5 days and then to room air. OIR-OTX008 group received an intravitreal injection of 1 μl (0.25 μg/μl) OTX008 at P12, OIR-PBS group received the equal volume (1 μl) of PBS injection. Mice from 4 groups were euthanized at P17, and retinas were collected for molecular biological analysis and morphological study. RNV was evaluated by counting the number of pre-retinal neovascular nuclei and the whole-mount immunofluorescent staining of mouse retina. Cyrosections of retinas were imaged via confocal microscopy to observe the enrichment of staining of Galectin-1. Protein levels of Galectin-1, Neuropilin-1 and phosphorylation of vascular endothelial growth factor receptor 2 (pVEGFR2) were determined with Western blot. Results At P17, Galectin-1 expressed higher in retinal ganglion cell layer, inner plexiform layer and inner nuclear layer from OIR group and OIR-PBS group than normal group. Galectin-1 expressed less in cryosection retinas from OIR-OTX008 group than OIR group and OIR-PBS group. The numbers of pre-retinal neovascular cell nuclei from OIR group and OIR-PBS group were obviously more than that from normal group (t=9.314,P<0.05). The number of pre-retinal neovascular cell nuclei from OIR-OTX008 group were obviously lower than those from OIR group and OIR-PBS group (t=8.038, 7.774;P<0.05). The RNV tufts area (t=13.250, 12.570), non-perfusion area (t=15.590, 12.430) and hypoxic area (t=9.542, 9.928) from OIR-OTX008 group were significantly smaller than those in OIR group and OIR-PBS group (P<0.05). Protein levels of Galectin-1 (t=24.800, 23.060), Neuropilin-1 (t=4.120, 3.530) and pVEGFR2 (t=25.880, 15.480) in the OIR-OTX008 group were significantly down-regulated than those from OIR group and OIR-PBS group (P<0.05). Conclusion Intravitreal injection of OTX008 inhibits RNV and ameliorates retinal hypoxia in mice model of OIR possibly through down-regulating Galectin-1, Neurolinpin-1 and pVEGFR2. Key words: Retinal neovascularization/prevention c Galectin 1/antagonists i Animal experimentation

SERUM GALECTIN-4 (GAL-4) IN PATIENTS WITH GASTRIC ADENOCARCINOMA: ACTIVE PLAYER IN THE FIELD.

21Feb 2017 SERUM GALECTIN-4 (GAL-4) IN PATIENTS WITH GASTRIC ADENOCARCINOMA: ACTIVE PLAYER IN THE FIELD. Ahmed Hamouda Arnaout and Lamya Mahmoud Ibrahim. Department of Internal Medicine, Faculty of Medicine, Zagazig University, Egypt. Department of Clinical Pathology, Faculty of Medicine, Mansoura University, Egypt.

Identification of functional SNPs in human LGALS3 gene by in silico analyses

BackgroundGalectin-3 protein, an S-type lectin, is encoded by LGALS3 gene. It consists of carbohydrate recognition domain (CRD), collagen like tandem repeats of nine amino acids and N-terminal 12-mer peptide. Its serum levels as well as some genetic variants were reported to be involved in various disease conditions like cancer, autoimmune diseases, heart diseases etc. Being viewed as an important molecule in biological responses and its association with various diseases, the present study was designed. This is the first in silico analyses of LGALS3. AimTo systematically explore the plausible effects of LGALS3 genetic variants on structure and functions of galectin-3. Material and methodsBoth sequence based and structure based approaches were adopted for analyses of non-synonymous single nucleotide polymorphisms (nsSNPs). Putative methylation and other post translational modifications were also analyzed using different tools. Muster and Swiss-PDB Viewer were used for modeling of predicted functional variants. ResultsOut of 1130 SNPs reported in dbSNP, only validated SNPs were chosen for analyses. A total of nine nsSNPs which included, 3 of N-terminal region and 6 of CRD encoding region, were found to have deleterious effect as predicted by various softwares. Analyses of regulatory SNPs predicted five functional SNPs in 3′UTR having putative miRNA binding sites and 3 intronic SNPs in potential transcription factor binding sites. ConclusionBased on these analyses, the present study suggested that the reported functional SNPs may act as potential targets in genetic association studies.

Galectin 1 secreted by mesenchymal stem cells blocks alfa synuclein in Parkinson Disease

Galectin 1 secreted by mesenchymal stem cells blocks alfa synuclein in Parkinson Disease

Novel biomarkers for cardiovascular risk prediction.

Cardiovascular disease (CVD) is the leading cause of death and disability worldwide. The primary prevention of CVD is dependent upon the ability to identify high-risk individuals long before the development of overt events. This highlights the need for accurate risk stratification. An increasing number of novel biomarkers have been identified to predict cardiovascular events. Biomarkers play a critical role in the definition, prognostication, and decision-making regarding the management of cardiovascular events. This review focuses on a variety of promising biomarkers that provide diagnostic and prognostic information. The myocardial tissue-specific biomarker cardiac troponin, high-sensitivity assays for cardiac troponin, and heart-type fatty acid binding proteinall help diagnose myocardial infarction (MI) in the early hours following symptoms. Inflammatory markers such as growth differentiation factor-15, high-sensitivity C-reactive protein, fibrinogen, and uric acid predict MI and death. Pregnancy-associated plasma protein A, myeloperoxidase, and matrix metalloproteinases predict the risk of acute coronary syndrome. Lipoprotein-associated phospholipase A2 and secretory phospholipase A2 predict incident and recurrent cardiovascular events. Finally, elevated natriuretic peptides, ST2, endothelin-1, mid-regional-pro-adrenomedullin, copeptin, and galectin-3 have all been well validated to predict death and heart failure following a MI and provide risk stratification information for heart failure. Rapidly developing new areas, such as assessment of micro-RNA, are also explored. All the biomarkers reflect different aspects of the development of atherosclerosis.

Renal carcinoma/kidney progenitor cell chimera organoid as a novel tumorigenesis gene discovery model.

ABSTRACTThree-dimensional (3D) organoids provide a new way to model various diseases, including cancer. We made use of recently developed kidney-organ-primordia tissue-engineering technologies to create novel renal organoids for cancer gene discovery. We then tested whether our novel assays can be used to examine kidney cancer development. First, we identified the transcriptomic profiles of quiescent embryonic mouse metanephric mesenchyme (MM) and of MM in which the nephrogenesis program had been induced ex vivo. The transcriptome profiles were then compared to the profiles of tumor biopsies from renal cell carcinoma (RCC) patients, and control samples from the same kidneys. Certain signature genes were identified that correlated in the developmentally induced MM and RCC, including components of the caveolar-mediated endocytosis signaling pathway. An efficient siRNA-mediated knockdown (KD) of Bnip3, Gsn, Lgals3, Pax8, Cav1, Egfr or Itgb2 gene expression was achieved in mouse RCC (Renca) cells. The live-cell imaging analysis revealed inhibition of cell migration and cell viability in the gene-KD Renca cells in comparison to Renca controls. Upon siRNA treatment, the transwell invasion capacity of Renca cells was also inhibited. Finally, we mixed E11.5 MM with yellow fluorescent protein (YFP)-expressing Renca cells to establish chimera organoids. Strikingly, we found that the Bnip3-, Cav1- and Gsn-KD Renca-YFP+ cells as a chimera with the MM in 3D organoid rescued, in part, the RCC-mediated inhibition of the nephrogenesis program during epithelial tubules formation. Altogether, our research indicates that comparing renal ontogenesis control genes to the genes involved in kidney cancer may provide new growth-associated gene screens and that 3D RCC-MM chimera organoids can serve as a novel model with which to investigate the behavioral roles of cancer cells within the context of emergent complex tissue structures.

Galectins: their network and roles in immunity/tumor growth control.

One route of realizing the information of glycans involves endogenous receptors (lectins). Occurrence at branch ends renders galactosides particularly accessible. Thus, they are suited for such a recognition process. Fittingly, these epitopes serve as physiological ligands. The ga(lactoside-binding) lectins share the β-sandwich fold with a sequence signature around a central tryptophan residue besides this specificity. Three modes of presentation of the carbohydrate recognition domain are known for galectins, and genome monitoring from fungi to mammals discloses that galectins form a network. The extent of its complexity varies considerably between organisms, for chicken reaching seven proteins, more for mammals. The current status of network analysis reveals overlapping and distinct expression profiles. Matching intra- and extracellular galectin presence, they have a broad range of functions at each site depending on their specific counterreceptor(s), with the possibility even for functional antagonism between family members. Orchestration of expression of galectin, the cognate glycan, its scaffold (protein or sphingolipid) and spatial aspects of glycoconjugate presentation has been detected to lead to growth regulation of immune and tumor cells. To delineate the factors that underlie the specificity of a galectin for its counterreceptor(s) in the cellular context and the details of structure-activity relationships by comparatively analyzing natural and rationally engineered proteins is the main challenge for ongoing research.

Research progress of the role of advanced glycation end products and their receptors in vascular calcification

Vascular calcification is a late complication of diabetes, atherosclerosis, and other diseases, which is a significant predictor of cardiovascular morbidity and mortality. Advanced glycation end products through their receptors, RAGE and Galectin-3, have great impacts on the transitions of microcalcification and macrocalcification, respectively, which lead to different clinical endpoints. It is particularly urgent to investigate the downstream derivatives of their receptor ligand signaling axes as well as to search for the intervention targeting the transmissison of calcification cascade. (Chin J Endocrinol Metab, 2016, 32: 872-875) Key words: Advanced glycation end products; Receptor for advanced glycation end products; Microcalcification; Macrocalcification