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.
OBJECTIVE This study was conducted to investigate ATP- induced growth inhibition in human leukemic cells KG1a. METHODS ATP inhibited cell growth was analyzed by MTS assay. Externalization of phosphatidylserine could be detected by Annexin-V-FITC apoptosis staining after activation of the P2X7 receptor. P2X7 mediated pore formation was detected in KGla cells by Yo-Pro-1 uptake assay. RESULTS ATP inhibited cell growth in a dose-dependent manner. The cytotoxic effect could be blocked by P2X7 antagonists, oxidized ATP （oATP） and KN62. Externalization of phosphatidylserine could be detected in a time-dependent manner. P2X7 mediated pore formation could be detected in KG1a cells. These effects could not be observed in P2X7 null Ramos cells. CONCLUSION The results and our previously reports that mRNA, protein expression and calcium response of the P2X7 receptor in KGla cells, suggested that extracellular ATP effectively induces growth inhibition through apoptosis in KGla cells by activation of P2X7 receptor, and that may be mediated by extracellular Ca^2＋ in ux and pore formation.
