| http://purl.uniprot.org/citations/22961085 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/22961085 | http://www.w3.org/2000/01/rdf-schema#comment | "Embryos exposed to high glucose exhibit aberrant maturational and cytoarchitectural cellular changes, implicating cellular organelle stress in diabetic embryopathy. c-Jun-N-terminal kinase 1/2 (JNK1/2) activation is a causal event in maternal diabetes-induced neural tube defects (NTD). However, the relationship between JNK1/2 activation and endoplasmic reticulum (ER) stress in diabetic embryopathy has never been explored. We found that maternal diabetes significantly increased ER stress markers and induced swollen/enlarged ER lumens in embryonic neuroepithelial cells during neurulation. Deletion of either jnk1 or jnk2 gene diminished hyperglycemia-increased ER stress markers and ER chaperone gene expression. In embryos cultured under high-glucose conditions (20 mmol/L), the use of 4-phenylbutyric acid (4-PBA), an ER chemical chaperone, diminished ER stress markers and abolished the activation of JNK1/2 and its downstream transcription factors, caspase 3 and caspase 8, and Sox1 neural progenitor apoptosis. Consequently, both 1 and 2 mmol/L 4-PBA significantly ameliorated high glucose-induced NTD. We conclude that hyperglycemia induces ER stress, which is responsible for the proapoptotic JNK1/2 pathway activation, apoptosis, and NTD induction. Suppressing JNK1/2 activation by either jnk1 or jnk2 gene deletion prevents ER stress. Thus, our study reveals a reciprocal causation of ER stress and JNK1/2 in mediating the teratogenicity of maternal diabetes."xsd:string |
| http://purl.uniprot.org/citations/22961085 | http://purl.org/dc/terms/identifier | "doi:10.2337/db12-0026"xsd:string |
| http://purl.uniprot.org/citations/22961085 | http://purl.uniprot.org/core/author | "Li X."xsd:string |
| http://purl.uniprot.org/citations/22961085 | http://purl.uniprot.org/core/author | "Xu C."xsd:string |
| http://purl.uniprot.org/citations/22961085 | http://purl.uniprot.org/core/author | "Yang P."xsd:string |
| http://purl.uniprot.org/citations/22961085 | http://purl.uniprot.org/core/date | "2013"xsd:gYear |
| http://purl.uniprot.org/citations/22961085 | http://purl.uniprot.org/core/name | "Diabetes"xsd:string |
| http://purl.uniprot.org/citations/22961085 | http://purl.uniprot.org/core/pages | "599-608"xsd:string |
| http://purl.uniprot.org/citations/22961085 | http://purl.uniprot.org/core/title | "c-Jun NH2-terminal kinase 1/2 and endoplasmic reticulum stress as interdependent and reciprocal causation in diabetic embryopathy."xsd:string |
| http://purl.uniprot.org/citations/22961085 | http://purl.uniprot.org/core/volume | "62"xsd:string |
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