Navegando por Palavras-chave "Células germinativas"

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    Papel de oct4, sox2 e caspase-3 na quiescência dos gonócitos de rato
    (Universidade Federal de São Paulo (UNIFESP), 2014-10-29) Arantes, Anelise Diniz [UNIFESP]; Teixeira, Taiza Stumpp Teixeira [UNIFESP]; Oliva, Samara Urban de [UNIFESP]; http://lattes.cnpq.br/5886968082690915; http://lattes.cnpq.br/1024329256080770; http://lattes.cnpq.br/0559069185165585; Universidade Federal de São Paulo (UNIFESP)
    Introduction: The germ cells emerge from the epiblast and migrate to the gonads, where they become gonocytes. The gonocytes are the precursors of the spermatogonial stem cells, but little is known about their differentiation. It is seems that the rigid control of gonocyte proliferation, quiescence and pluripotent marker expression is crucial for germ cell development. Objective: Identify the pre-natal period of male germ cell quiescence in the rat and whether caspase-3 (Casp3) is involved in the process. Methods: Rat embryonic gonads were collected at 15, 17 and 19 days post-coitum (dpc). The expression of pluripotency (SOX2, OCT4) and proliferation (Ki67, phosphorylated Retinoblastoma 1 (pRb1)) markers as well as of cleaved Casp3 was analysed. To address Casp3 role in rat gonocyte quiescence, testes from 19dpc embryos were incubated with Casp3 inhibitor and submitted to the immunolabelling of Ki67, PCNA, Casp3 and NANOG. Results: The number of Ki67 and pRB1-labelled gonocytes reduced from 15dpc to 17dpc reaching zero at 19dpc, indicating that quiescence starts around 15dpc and that they are quiescent at 19dpc. OCT4 labelling followed the same detection pattern, whereas SOX2 was present only at 15dpc. These data suggest that the establishment of the quiescence period involves the downregulation of these pluripotent markers. Casp3 labelling was opposite to OCT4, pRB1 and Ki67 labelling, suggesting that it has a role in rat gonocyte quiescence. Casp3 labelling was maintained after the incubation with Casp3 inhibitor, what was expected since the inhibitor does not induce Casp3 degradation. Ki67 was not detected in the gonads incubated with Casp3 inhibitor, suggesting that Caps3 inhibition does not reactivate the cell cycle. NANOG was detected in the gonocyte cytoplasm at 19dpc and its labelling was identical to that of Casp3, suggesting that it has a role in the control of germ cell cycle in the embryo and may interact with Casp3. PCNA-positive and negative gonocytes were observed in 19dpc gonads before and after culture. However, the number of PCNA-negative gonocytes increased in the gonads incubated with Casp3-inhibitor, suggesting that Casp3 is a positive regulator of PCNA. Conclusion: These results suggest that OCT4 and SOX2 downregulation as well as Casp3 and NANOG expression are involved in rat gonocyte quiescence and that PCNA depend on Casp3 activity in these cells.