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Correlation between spina bifida manifesta in fetal rats and c-Jun N-terminal kinase signaling

Correlation between spina bifida manifesta in fetal rats and c-Jun N-terminal kinase signaling
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摘要 Fetal rat models with neural tube defects were established by injection with retinoic acid at 10 days after conception. The immunofluorescence assay and western blot analysis showed that the number of caspase-3 positive cells in myeloid tissues for spina bifida manifesta was increased. There was also increased phosphorylation of c-Jun N-terminal kinase, a member of the mitogen activated protein kinase family. The c-Jun N-terminal kinase phosphorylation level was positively correlated with caspase-3 expression in myeloid tissues for spina bifida manifesta. Experimental findings indicate that abnormal apoptosis is involved in retinoic acid-induced dominant spina bifida formation in fetal rats, and may be associated with the c-Jun N-terminal kinase signal transduction pathway. Fetal rat models with neural tube defects were established by injection with retinoic acid at 10 days after conception. The immunofluorescence assay and western blot analysis showed that the number of caspase-3 positive cells in myeloid tissues for spina bifida manifesta was increased. There was also increased phosphorylation of c-Jun N-terminal kinase, a member of the mitogen activated protein kinase family. The c-Jun N-terminal kinase phosphorylation level was positively correlated with caspase-3 expression in myeloid tissues for spina bifida manifesta. Experimental findings indicate that abnormal apoptosis is involved in retinoic acid-induced dominant spina bifida formation in fetal rats, and may be associated with the c-Jun N-terminal kinase signal transduction pathway.
出处 《Neural Regeneration Research》 SCIE CAS CSCD 2012年第32期2485-2491,共7页 中国神经再生研究(英文版)
基金 supported by the National Natural Science Foundation of China, No.30872705/HD426 and No.81070538/HD429
关键词 retinoic acid neural tube defects myeloid tissues caspase-3 apoptotic kinase c-Jun N-terminal kinase mitogen-activated protein kinase neural development REGENERATION neural regeneration retinoic acid neural tube defects myeloid tissues caspase-3 apoptotic kinase c-Jun N-terminal kinase mitogen-activated protein kinase neural development regeneration neural regeneration
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