ABSTRACT
Mammalian oocytes within Graafian follicles are arrested at prophase I of meiosis. C-type natriuretic peptide (NPPC), secreted by mural granulosa cells (MGCs), maintains oocyte meiotic arrest via binding to its cognate receptor natriuretic peptide receptor 2 (NPR2) and producing cyclic guanosine monophosphate (cGMP). NPR2 is most concentrated in the cumulus cells. In addition, cAMP, gap junction, inosine monophosphate dehydrogenase (IMPDH) and other important regulatory factors are also involved in meiotic arrest. Luteinizing hormone (LH) then rapidly decreases cGMP and induces oocyte meiotic resumption. In this paper, advances in the molecular mechanisms of meiotic arrest and LH-induced meiotic resumption were reviewed. This paper may provide new ideas for the prevention, diagnosis and treatment of related reproductive diseases.
Subject(s)
Luteinizing Hormone , Oocytes , Animals , Cumulus Cells , Female , Meiosis , Natriuretic Peptide, C-Type/geneticsABSTRACT
AIM: To study the effect of puerarin on vascular endothelial cells apoptosis induced by chemical hypoxia-ischemia in vitro. METHODS: The chemical hypoxia-ischemia model was performed by treating cultured bovine aortic endothelial cells (BAECs) with NaCN in glucose-free medium. Cell viability was determined by trypan blue staining. Cell apoptosis was defined by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL), flow cytometry and Hoechst 33342 staining. The expression of Caspase-3 in endothelial cells was detected by immunocytochemical method. RESULTS: Chemical hypoxia-ischemia was shown to initiate bovine aortic endothelial cell apoptosis. Puerarin (0.5-3 mmol.L-1) was found to inhibit endothelial cell apoptosis effectively, and reduce the expression of Caspase-3 significantly. CONCLUSION: Puerarin can protect apoptotic endothelial cells induced by chemical hypoxia-ischemia markedly and the effect was performed partly by decreasing Caspase-3 expression.
Subject(s)
Apoptosis , Endothelium, Vascular/drug effects , Isoflavones/pharmacology , Protective Agents/pharmacology , Animals , Aorta, Thoracic/cytology , Caspase 3 , Caspases/metabolism , Cattle , Cell Hypoxia/drug effects , Cells, Cultured , DNA Damage/drug effects , Endothelium, Vascular/cytologyABSTRACT
AIM: To study the effects of caspases on cerebromicrovascular endothelial cell apoptosis induced by hypoxia in vitro. METHODS: The cultured bovine cerebromicrovascular endothelial cells were exposed to NaCN in glucose-free medium. Cell viability was determined by trypan blue staining. Cell apoptosis was defined by terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) and flow cytometry. The expression of caspase-3 was detected by immunocytochemical method. Four caspase inhibitors were used to validate the effect of caspases on cell apoptosis. RESULTS: NaCN in glucose-free medium initiated cerebromicrovascular endothelial cell injury markedly and typical apoptotic cells were found in this model. The expression of caspase-3 increased significantly. Four caspase inhibitors decreased the number of injured cells. Selective inhibitor of caspase-1 and -6 reduced expression of caspase-3 significantly. CONCLUSION: The results suggest that caspases family plays an important role in cerebromicrovascular endothelial cell apoptosis induced by NaCN and caspase-3 acts on the downstream of caspase-1 and -6 in protease cascade action to induce apoptosis.