Serum Follistatin Level Research Articles

Serum follistatin level as a prognostic marker in Haploidentical stem cell transplantation

BackgroundThe treatment of hematological diseases with Haploidentical transplantation has made significant progress. Follistatin is an angiogenic factor that is elevated in the circulation after allogeneic Hematopoietic Cell Transplantation (HCT). Elevated follistatin levels have been linked to poor survival after graft versus host disease (GVHD). ObjectivePre- and post-transplant Follistatin levels were measured in patients subjected to Haploidentical HSCT and correlated with transplant outcomes. Patients and methodsThis study included 45 patients who underwent allogeneic stem cell transplants from Haploidentical donors. ResultsThe mean Follistatin level before stem cells infusion (88.81 ± 49.11 ng/ml) and at day 28 post-transplant (78.61 ± 45.50 ng/ml). The mean follistatin level was higher among the patients who had acute severe GVHD grade 3–4 pre-transplant at day zero and day 28 without statistical significance.The incidence of veno-occlusive disease was higher in patients with elevated serum follistatin levels on day 0 (108.58 ± 64.12 Vs 82.16 ± 46.05 ng/ml. p value = 0.134) and day 28 (112 ± 49.36 vs 66.06 ± 38.96 ng/ml) with statistically significance at day 28 post-transplant (p value = 0.011).After 180 days of follow-up, patients with high serum follistatin (i.e. >60 ng/ml) on day 28 post-transplant had lower OS, (P = 0.381). ConclusionIn the setting of Haploidentical HSCT, higher follistatin levels post-transplant are associated with severe acute GVHD and inferior overall survival.

The association of the serum levels of myostatin, follistatin, and interleukin-6 with sarcopenia, and their impacts on survival in patients with hepatocellular carcinoma.

Background/AimsThe role of serum myokine levels in sarcopenia and the outcome of hepatocellular carcinoma (HCC) patients are not clear. This study investigated the serum levels of myostatin, follistatin, and interleukin-6 (IL-6) in HCC patients and their association with sarcopenia and survival.MethodsUsing prospectively collected pretreatment samples from 238 HCC patients in a hospital from 2012 to 2015, the serum levels of 3 myokines were determined and compared to 50 samples from age and sex-matched healthy controls. Sarcopenia was evaluated using the psoas muscle index (PMI) measured at the third lumbar level in the computed tomography, and clinical data were collected until 2017.ResultsThe median levels of the 3 myokines for the male and female HCC patients were as follow: myostatin (3,979.3 and 2,976.3 pg/mL), follistatin (2,118.5 and 2,174.6 pg/mL), and IL-6 (2.5 and 2.7 pg/mL), respectively. Those in the HCC patients were all significantly higher than in the healthy controls. In the HCC patient, the median PMI was 4.43 (males) and 2.17 cm2/m2 (females) with a sarcopenic prevalence of 56.4%. The serum levels of myostatin, IL-6 and follistatin in the HCC patients showed a positive, negative, and no correlation with PMI, respectively. The serum follistatin level was an independent factor for poor survival in HCC patients.ConclusionsThe serum levels of myostatin, follistatin, and IL-6 and their correlation with sarcopenia and survival were presented in HCC patients for the first time. The role of the serum follistatin level as a poor prognostic biomarker warrants further study.

Assessment of follistatin level in atherosclerosis patients and its relation with some anthropometric criterion as predictor survival

Follistatin (FST) is glycoprotein, otherwise called activin restricting protein, is an endogenously created protein that ties activin A with high fondness and restrains its bioactivity. The essential capacity of FST is the authoritative and bioneutralization of individuals from the TGF-β superfamily and activin A specifically. FST advances adipogenic separation of begetter cells. FST has been embroiled in aggravation and renovating, any adjustment in the level of FST, which might be a determinant of the seriousness of irritation, or tissue phenotypic change. Atherosclerosis is a dynamical procedure that rises up out of the interchange between lipid digestion, irritation and inborn insusceptibility. The blood vessel area of atherosclerosis makes it strategically and morally hard to think about in vivo. To enhance our comprehension of the infection, we should discover elective approaches to research its movement. The points of this investigation; we need to know the connection between the serum FST level with atherosclerosis malady and its relationship with some deliberate rule, for example, sex, age, BMI, waist circumference and smoking.

Increased follistatin associated with decreased gait speed among old adults.

Low gait speed is associated with inflammation and muscle strength. Follistatin, a glycosylated plasma protein, is involved in inflammatory diseases, bone metabolism, muscle strength and cognition. However, research regarding the relationship between follistatin and gait speed in elderly individuals is limited. In this study, we aimed to examine the association between follistatin and gait speed in older adults. This cross-sectional, observational study included 205 ambulatory individuals aged ≥ 65 years. The baseline measures included 15-foot walking time, a structured questionnaire, grip strength and biomarkers, including follistatin and myostatin levels. Multiple linear regression was used to determine the change in gait speed for each 1 pg/mL increase in serum follistatin level. An extended model approach with a quartile-based analysis of serum follistatin levels was conducted. In the linear regression model, the β coefficient, representing the change in gait speed for each 1 pg/mL increase in serum follistatin level, was -0·308 (P < 0·001). After additional adjustment for relevant covariates, the β coefficient changed slightly, although the negative correlation remained (all P ≤ 0·001). After controlling for multiple covariates, participants in the highest serum follistatin level quartile had a significantly lower gait speed than those in the lowest quartile (all P for trend < 0·001). A higher follistatin level was independently associated with lower gait speed in community-dwelling elderly individuals; this suggests that serum follistatin level may be an indicator of mobility in elderly persons and may more particularly represent lower extremity function.

Serum Levels of Follistatin Are Positively Associated With Serum-Free Thyroxine Levels in Patients With Hyperthyroidism or Euthyroidism.

Follistatin is a glycoprotein with various biologic functions that plays a role in adipocyte differentiation, muscle stimulation, anti-inflammation, and energy homeostasis. Thyroid hormones influence energy expenditure, glucose, and lipid metabolism. The association between serum follistatin level and thyroid function statuses has seldom been evaluated.The objectives of this study were to compare serum follistatin concentrations in different thyroid function statuses and to evaluate the associations between serum follistatin and free thyroxine (fT4) levels.In this study, 30 patients with hyperthyroidism (HY group) and 30 euthyroid individuals (EU group) were recruited. The patients of HY group were treated with antithyroid regimens as clinically indicated, whereas no medication was given to EU group. The demographic and anthropometric characteristics, biochemical data, serum levels of follistatin, and thyroid function of both groups at baseline and at the 6th month were compared. Data of all patients were pooled for the analysis of the associations between the levels of follistatin and fT4.At baseline, the HY group had significantly higher serum follistatin levels than the EU group (median [Q1, Q3]: 1.81 [1.33, 2.78] vs 1.13 [0.39, 1.45] ng/mL, P < 0.001). When treated with antithyroid regimens, the follistatin serum levels in HY group decreased to 1.54 [1.00, 1.88] ng/mL at the 6th month. In all patients, the serum levels of follistatin were positively associated with fT4 levels at baseline (β = 0.54, P = 0.005) and at the 6th month (β = 0.59, P < 0.001). The association between follistatin and fT4 levels remained significant in the stepwise multivariate regression analysis, both initially and at the 6th month.In comparison to the EU group, patients with hyperthyroidism had higher serum follistatin levels, which decreased after receiving antithyroid treatment. In addition, the serum follistatin concentrations were positively associated with serum fT4 levels in patients with hyperthyroidism or euthyroidism.

O-004 Serum Follistatin In Girls With Pubertal Hyperandrogenism

The aim of the study was to examine the serum follistatin level in adolescent girls with hyperandrogenism (HA) and its possible role in the development of ovarian dysfunction. Methods Follistatin, follicle-stimulating hormone (FSH), estradiol (E 2 ) were studied in serum of 42 adolescent girls aged 15–17 years with different clinical symptoms of HA (acne, hirsutism) and irregular menstrual cycle (IMC), 42 patients with regularmenstrual cycle (RMC) and 30 healthy adolescents. Results Hyperandrogenic patients with IMC showed an increased follistatin secretion (p? =0,03) compared to a group with RMC and control group. This fact points to the involvement of this glycoprotein in the pathogenesis of ovarian dysfunctionin girls’ puberty. Also we found significant negative correlation between the levels of FSH and follistatin (p = 0,02) that proved the inverse relationship between secretion of gonadotropins and follistatin level. Besides the negative correlation between follistatin and E 2 has been revealed (p = 0,04). Conclusions It may be difficult to distinguish biologically and ultrasonically hyperandrogenic adolescents as the result of normalmaturational process of puberty from the ones with developing polycystic ovarian syndrome (PCOS). The increased secretion of follistatin and its correlation with the reduction of FSH and estradiol in adolescent girls with menstrual irregularities and hyperandrogenism confirms the pathological role of this intraovarian factor in discoordination of peripheral functioning of reproductive system, and its possible significance in pathogenesis of PCOS as a future outcome of pubertal hyperandrogenism.

High Serum Levels of Follistatin in Patients with Ovarian Cancer

This study investigated the potential use of serum follistatin (FST) as a marker for ovarian cancer alongside serum cancer antigen-125 (CA-125). Serum samples were collected from patients with ovarian cancer (n = 45), benign ovarian cysts (n = 40) or other cancers (n = 100) and from healthy subjects (n = 60) for the determination of FST and CA-125 levels using enzyme-linked immunosorbent assays. Expression of FST in ovarian tissue was investigated using immunohistochemical staining. Compared with healthy subjects and patients with benign ovarian cysts, serum FST and CA-125 levels were significantly increased in patients with ovarian cancer. Using the 95% confidence interval for the healthy subjects group as the cut-off value, tumour marker sensitivity and specificity in ovarian cancer were 53.3% and 97% for FST and 77.8% and 84% for CA-125, respectively. Tissue expression of FST protein was more pronounced in ovarian cancer than in normal ovary. The serum FST level was elevated in the peripheral blood of patients with ovarian cancer and has potential as a tumour marker for ovarian cancer diagnosis. It may be particularly useful when combined with CA-125 detection to reduce the number of false-positive results.

Serum follistatin level as an early detection marker of post-hepatectomy liver failure: Using our novel rat 90% hepatectomy model

Serum follistatin level as an early detection marker of post-hepatectomy liver failure: Using our novel rat 90% hepatectomy model

Serum follistatin level as an early detection marker of post-hepatectomy liver failure: Using our novel rat 90% hepatectomy model

Serum follistatin level as an early detection marker of post-hepatectomy liver failure: Using our novel rat 90% hepatectomy model

Production of follistatin in porcine endothelial cells: differential regulation by bacterial compounds and the synthetic glucocorticoid RU 28362.

Follistatin (FS) is the specific binding protein of activin; it has a broad tissue distribution and is also found in serum. The ovary has the highest level of FS expression, but ovariectomy does not cause a permanent reduction in the serum FS level. Therefore, the source of FS in serum is still elusive. As a regulatable, nongonadal source of serum FS could influence ovarian and pituitary-derived hormone secretion and thus reproductive function, we searched for a source of extragonadal FS expression that might contribute to the FS protein level in serum. We found that endothelial cells from blood vessels express FS messenger RNA (mRNA) and protein; therefore, we studied the regulation of steady state levels of FS mRNA in porcine endothelial cells from aorta (AEC) and brain microvessels (BMVEC) in tissue culture. For detection of FS mRNA, a specific 32P-radiolabeled antisense probe and a S1-nuclease protection assay were used. FS steady state levels of AEC decreased with time in culture, i.e. postconfluent AEC had lower FS mRNA levels than confluent cultures, which, in turn, had lower FS mRNA levels than subconfluent cell cultures. FS mRNA levels in AEC were induced by increasing concentrations of FCS and stimulated by 30 micrograms/ml endothelial cell growth supplement. FS mRNA levels in AEC and BMVEC increased approximately 20-fold within 4 h during incubation of the cells with 100 nM phorbol 12-myristate, 13-acetate, whereas 0.5 nmol/ml forskolin tested in AEC for between 4-48 h had no significant effect. Furthermore, 0.1 microM ocadaic acid, an inhibitor of serine/threonine phosphatases 1 and 2A, caused a significant increase in FS mRNA levels. FS mRNA levels in AEC were not significantly affected by various concentrations of porcine FSH, epidermal growth factor, or retinoic acid for between 4-48 h. Treatment of the cells with 0.01-10 micrograms/ml bacterial lipopolysaccharides (LPS) caused a dose-dependent increase (up to 10-fold) in FS mRNA steady state level in AEC, whereas 1-1000 nM RU 28362, a synthetic glucocorticoid, inhibited FS mRNA steady state levels in a dose-dependent manner. The induction of FS mRNA with 1 microgram/ml LPS was completely blocked by 100 nM RU 28362, and the stimulatory effects of LPS were only visible after 4 h of treatment, not after 24 or 48 h. The same effects were observed with BMVEC. We, furthermore, analyzed FS protein secretion of AEC by Western blotting and demonstrated that FS proteins were secreted into the culture medium upon stimulation with LPS. None of these treatments had an obvious effect on the ratio of the two different forms of FS mRNA (FS 344:FS 317). Besides the expression of FS mRNA in AEC and BMVEC, FS mRNA is also expressed in uncultured plexus choroideus epithel and meninges, and FS protein is found in human cerebrospinal fluid. From this study it is concluded that 1) endothelial cells from different tissues produce FS mRNA; 2) the FS mRNA levels of AEC and BMVEC are subjected to regulation by FCS, endothelial cell growth supplement, bacterial LPS, and the glucocorticoid RU 28362; 3) phosphatases and the protein kinase C-dependent, but not the protein kinase A-dependent, pathway are involved in regulating the steady state levels of FS mRNA in AEC and BMVEC; and 4) endothelial cells produce and secrete FS protein and are thus a likely source of FS in serum.

Immunoradiometric assay for follistatin: serum immunoreactive follistatin levels in normal adults and pregnant women.

A sensitive and specific immunoradiometric assay for follistatin was developed using antifollistatin mouse monoclonal and rabbit polyclonal antibodies. The sensitivity of the assay was 0.5 micrograms/L, and cross-reactivities with recombinant human activin A and bovine inhibin were less than 0.1%. The intra- and interassay coefficients of variation were less than 10%, and the recovery rate was about 90% in human serum. The addition of activin A to the same sample resulted in a minimal influence on follistatin recovery, indicating that this assay system can measure the total level of activin-bound and unbound follistatin. Gel filtration analysis of human serum showed that the majority of immunoreactivity was eluted in a larger molecular size position than that of free follistatin, suggesting that the large part of follistatin is bound to other proteins, presumably activins, in serum. Using this assay, immunoreactive follistatin levels in various biological fluids and human sera were examined. The dose-response curves of porcine follicular and amniotic fluids were parallel to the standard curve, and porcine follicular fluid contained extremely high follistatin immunoreactivity (5.6 mg/L). The serum follistatin level in normal human volunteers was 13.3 +/- 4.7 micrograms/L (mean +/- SD; n = 60), with a tendency to increase gradually with age. On the other hand, the serum follistatin level was remarkably elevated in pregnant women (62.7 +/- 35.3 micrograms/L; n = 57), with a positive correlation with weeks of pregnancy. These data indicated that circulating immunoreactive follistatin is detectable in human serum, and the levels vary with physiological conditions such as aging and pregnancy.