GATA4 (Phospho-Ser262) ELISA Kit

Introduction: The emergence of numerous tissue engineering and regenerative medicine techniques cell encapsulation paves a way to heal and restore the function of various injured tissues mainly cardiovascular system. Here, we aimed to investigate the role of alginate-gelatin encapsulation on the dynamic of rat cardiomyoblasts in vitro. Materials and methods: Rat cardiomyoblasts cell line H9C2 were enclosed by using alginate-gelatin microspheres and incubated for 7 days. MTT method was used to examine cell viability. The level of genes associated with cardiomyoblasts maturation MYL7, NPPA, NKX2-5, and GATA4 real-time PCR. ELISA was used to measure the protein levels of Bcl-2 and Bax factor post-encapsulation. The level of SOD, GPx, and TAC was detected by biochemical analyses. Western blotting was performed to measure the content of AMP-activated protein kinase. Results: We found that encapsulation was able to increase the viability of rat cardiomyocytes after 7 days. The decreased level of Bcl-2 (p < 0.001) coincided with non-significant differences in the level of Bax (p > 0.05). The transcription level of all genes MYL7, NPPA, NKX2-5, and GATA4 were found to down-regulate compared to the control non-treated cells (p < 0.05). No significant differences were found regarding the level of SOD, GPx, and TAC compared to the control (p > 0.05). According to western blotting, revealed a reduced level of AMPK following 7-day incubation of rat cardiomyoblasts (p < 0.05). Conclusion: Data confirmed that the encapsulation of rat cardiomyoblasts with alginate-gelatin microspheres maintained the cells multipotentiality.

Background: Aberrant signaling between germ cells and somatic cells can lead to reproductive disease and depends on diffusible signals, including transforming growth factor-beta (TGFB) -family proteins. The TGFB-family protein Gsdf (gonadal soma derived factor) controls sex determination in some fish and is a candidate for mediating germ cell/soma signaling. Results: Zebrafish expressed gsdf in somatic cells of bipotential gonads and expression continued in ovarian granulosa cells and testicular Sertoli cells. Homozygous gsdf knockout mutants delayed leaving the bipotential gonad state, but then became a male or a female. Mutant females ovulated a few oocytes, then became sterile, accumulating immature follicles. Female mutants stored excess lipid and down-regulated aromatase, gata4, insulin receptor, estrogen receptor, and genes for lipid metabolism, vitellogenin, and steroid biosynthesis. Mutant females contained less estrogen and more androgen than wild-types. Mutant males were fertile. Genomic analysis suggests that Gsdf, Bmp15, and Gdf9, originated as paralogs in vertebrate genome duplication events. Conclusions: In zebrafish, gsdf regulates ovarian follicle maturation and expression of genes for steroid biosynthesis, obesity, diabetes, and female fertility, leading to ovarian and extra-ovarian phenotypes that mimic human polycystic ovarian syndrome (PCOS), suggesting a role for a related TGFB signaling molecule in the etiology of PCOS. Developmental Dynamics 246:925-945, 2017. (c) 2017 Wiley Periodicals, Inc.