Spermatogenesis is a complicated and poorly understood process that relies on the precise regulation of the self-renewal and differentiation of spermatogonia. In many organisms, micro RNAs(mi RNAs) are involved in multiple developmental processes as critical regulators of transcriptional and post-transcriptional gene silencing. This study investigated the expression pattern of mi RNAs in type B spermatogonia cells(BSc) and primary spermatocytes(PSc) of mice, using a high-throughput small RNA sequencing system. The results revealed that the expression levels of Let-7 family mi RNAs were remarkably high in both cell types. Furthermore, the expression levels of mi R-21, mi R-140-3p, mi R-103, mi R-30 a, mi R-101 b and mi R-99 b were decreased during the transformation from BSc to PSc. These mi RNAs target vital genes that participate in apoptosis, cell proliferation and differentiation, junction assembly and cell cycle regulation. These results highlight the indispensable role of mi RNAs in spermatogenesis.
This study was conducted to investigate ATP-induced growth inhibition in human leukemic cells KGla.METHODS ATP inhibited cell growth was analyzed by MTSassay.Externalization of phosphatidylserine could be detected byAnnexin-V-FITC apoptosis staining after activation of the P2X7 re-ceptor.P2X7 mediated pore formation was detected in KGla cellsby Yo-Pro-1 uptake assay.RESULTS ATP inhibited cell growth in a dose-dependent man-ner.The cytotoxic effect could be blocked by P2X7 antagonists,oxidized ATP (oATP) and KN62.Externalization of phosphatidyl-serine could be detected in a time-dependent manner.P2X7 medi-ated pore formation could be detected in KGla cells.These effectscould not be observed in P2X7 null Ramos cells.CONCLUSIONThe results and our previously reports thatmRNA,protein expression and calcium response of the P2X7receptor in KGla cells,suggested that extracellular ATP effectivelyinduces growth inhibition through apoptosis in KGla cells byactivation of P2X7 receptor,and that may be mediated by extracel-lular Ca^(2+)in@ux and pore formation.
