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dc.contributor.authorWu, Hung-Yien_US
dc.contributor.authorLin, Chia-Yingen_US
dc.contributor.authorLin, Tze-Yien_US
dc.contributor.authorChen, Tai-Changen_US
dc.contributor.authorYuan, Chiun-Jyeen_US
dc.date.accessioned2014-12-08T15:12:40Z-
dc.date.available2014-12-08T15:12:40Z-
dc.date.issued2008-02-01en_US
dc.identifier.issn1360-8185en_US
dc.identifier.urihttp://dx.doi.org/10.1007/s10495-007-0161-xen_US
dc.identifier.urihttp://hdl.handle.net/11536/9735-
dc.description.abstractThe placenta is essential in transferring gases and nutrients from the mother to the developing fetus. Trophoblast apoptosis may cause labor or other pregnancy-related disorders. This study demonstrated the essential role of Mst3, a human Ste20-like protein kinase, in the oxidative stress-induced apoptosis of trophoblasts of term placenta in normal spontaneous delivery. Oxidative stress, but not hormones released during labor such as prostaglandin E-1, oxytocin or angiotensin II, induces the expression of Mst3 and apoptosis of human term placenta after elective Cesarean section without labor pain. The role of Mst3 in oxidative stress-induced apoptosis was further demonstrated in the 3A-sub-E, a human trophoblast cell line. The H2O2-induced apoptosis of 3A-sub-E cells was largely suppressed by overexpressed Mst3(KR), the kinase-dead mutant or by selective knockdown of endogenous Mst3. Further studies showed that Jun N-terminal kinase (JNK) may participate in the signaling pathway of H2O2-induced apoptosis by mediating the level of Mst3. Subsequently, caspase 3 and other downstream apoptotic components may be activated by Mst3 and trigger the apoptotic process in human trophoblasts.en_US
dc.language.isoen_USen_US
dc.subjectMst3en_US
dc.subjectoxidative stressen_US
dc.subjectplacentaen_US
dc.subjecttrophoblastsen_US
dc.subjectapoptosisen_US
dc.subjectparturitionen_US
dc.titleMammalian Ste20-like protein kinase 3 mediates trophoblast apoptosis in spontaneous deliveryen_US
dc.typeArticleen_US
dc.identifier.doi10.1007/s10495-007-0161-xen_US
dc.identifier.journalAPOPTOSISen_US
dc.citation.volume13en_US
dc.citation.issue2en_US
dc.citation.spage283en_US
dc.citation.epage294en_US
dc.contributor.department生物科技學系zh_TW
dc.contributor.departmentDepartment of Biological Science and Technologyen_US
dc.identifier.wosnumberWOS:000252797000009-
dc.citation.woscount18-
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