Rat Carbonic Anhydrase II ELISA Kit

The spermatozoon is a highly differentiated cell with unique characteristics: it is mobile, thanks to its flagellum, and is very compact. The sperm cytoplasm is extremely reduced, containing no ribosomes, and therefore does not allow translation, and its nucleus contains very closed chromatin, preventing transcription. This DNA compaction is linked to the loss of nucleosomes and the replacement of histones by protamines. Based on these characteristics, sperm was considered to simply deliver paternal DNA to the oocyte. However, some parts of the sperm DNA remain organized in a nucleosomal format, and bear epigenetic information. In addition, the nucleus and the cytoplasm contain a multitude of RNAs of different types, including non-coding RNAs (ncRNAs) which also carry epigenetic information. For a long time, these RNAs were considered residues of spermatogenesis. After briefly describing the mechanisms of compaction of sperm DNA, we focus this review on the origin and function of the different ncRNAs. We present studies demonstrating the importance of these RNAs in embryonic development and transgenerational adaptation to stress. We also look at other epigenetic marks, such as DNA methylation or post-translational modifications of histones, and show that they are sensitive to environmental stress and transmissible to offspring. The post-fertilization role of certain sperm-borne proteins is also discussed.

Background: Our previous study suggested that palmitate (PA) induces human glomerular mesangial cells (HMCs) fibrosis. However, the mechanism is not fully understood. Recent studies suggested that transient receptor potential canonical channel 6 (TRPC6)/nuclear factor of activated T cell 2 (NFAT2) played an important role in renal fibrosis. Moreover, cluster of differentiation 36 (CD36) regulated the synthesis of TPRC6 agonist diglyceride. In the present study, we investigated whether PA induced HMCs fibrosis via TRPC6/NFAT2 mediated by CD36. Methods: A type 2 diabetic nephropathy (DN) model was established in Sprague Dawley rats, and HMCs were stimulated with PA. Lipid accumulation and free fatty acid (FFA) uptake were measured. The expression levels of TGF-beta 1, p-Smad2/3, FN, TRPC6, NFAT2 and CD36 were evaluated. The intracellular calcium concentration ([Ca2+]i) was assessed. Results: FFA were elevated in type 2 DN rats with kidney fibrosis in addition to NFAT2 and CD36 expression. In vitro, PA induced HMCs fibrosis, [Ca2+](i) elevation and NFAT2 activation. SKF96365 or TRPC6-siRNA could attenuate PA-induced HMCs damage. By contrast, the TRPC6 activator showed the opposite effect. Moreover, NFAT2-siRNA also suppressed PA-induced HMCs fibrosis. CD36 knockdown inhibited the PA-induced [Ca2+](i) elevation and NFAT2 expression. In addition, long-term treatment with PA decreased TRPC6 expression in HMCs. Conclusion: The results of this study demonstrated that PA could induce the activation of the [Ca2+](i)/NFAT2 signaling pathway through TRPC6, which led to HMCs fibrosis. Although activation of TRPC6 attributed to CD36-mediated lipid deposition, long-term stimulation of PA may lead to negative feedback on the expression of TPRC6.