ArticleThe journal of maternal-fetal & neonatal medicine : the official journal of the European Association of Perinatal Medicine, the Federation of Asia and Oceania Perinatal Societies, the International Society of Perinatal Obstetricians2012
The essential role of protein kinase Cδ in diabetes-induced neural tube defects.
Article in The journal of maternal-fetal & neonatal medicine : the official journal of the European Association of Perinatal Medicine, the Federation of Asia and Oceania Perinatal Societies, the International Society of Perinatal Obstetricians, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- Exploring Research Trends and Mechanisms: Maternal Diabetes and Neural Tube Defects (1991-2023).Journal of multidisciplinary healthcare · 2025Article
- Ectopic Lipid Accumulation Correlates with Cellular Stress in Rabbit Blastocysts from Diabetic Mothers.International journal of molecular sciences · 2023Article
- Tip60- and sirtuin 2-regulated MARCKS acetylation and phosphorylation are required for diabetic embryopathy.Nature communications · 2019Article
- Reevaluation of Antioxidative Strategies for Birth Defect Prevention in Diabetic Pregnancies.Journal of biomolecular research & therapeutics · 2016Article
- The status of diabetic embryopathy.Upsala journal of medical sciences · 2016Review
- Identification of novel cell survival regulation in diabetic embryopathy via phospholipidomic profiling.Biochemical and biophysical research communications · 2016Article
- Curcumin ameliorates high glucose-induced neural tube defects by suppressing cellular stress and apoptosis.American journal of obstetrics and gynecology · 2015Article
- Genetic, epigenetic, and environmental contributions to neural tube closure.Annual review of genetics · 2014Review
- New concepts in diabetic embryopathy.Clinics in laboratory medicine · 2013Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
backgroundMaternal diabetes causes neural tube defects (NTDs) in the embryos via activating protein kinase Cs (PKCs), which regulate programmed cell death (apoptosis). The aims of this study are to investigate the role of proapoptotic PKCδ in NTD formation and the underlying mechanisms.
methodsPKCδ heterozygous (pkcδ(+/-)) female mice were diabetic (DM) induced by intravenous injection of streptozotocin. Occurrence of NTDs was evaluated at embryonic day 11.5 and compared between wild type (WT) and PKCδ homozygous (pkcδ(-/-)) embryos. Changes in oxidative and endoplasmic reticulum (ER) stress-associated factors and stress-response c-Jun N-terminal kinases (JNKs) were assessed using Western blot assay.
resultsCompared to DM/WT, the DM/PKCδ(-/-) embryos had significantly lower NTD rate and lower levels of oxidative and ER stress factors and JNK activation. These values were similar to those in the non-diabetic control group.
conclusionPKCδ plays a critical role in diabetes-induced NTDs, potentially through increasing oxidative and ER stress and JNK-associated stress-response pathways.
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Registered trials
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