Altered protein kinase C activation associated with rat embryonic dysmorphogenesis
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Updated: Aug 21, 2026

Light-mediated Reversible Modulation of the Mitogen-activated Protein Kinase Pathway during Cell Differentiation and Xenopus Embryonic Development
Published on: June 15, 2017
Mattias Gäreskog1, Parri Wentzel
1Department of Medical Cell Biology, Uppsala University, Biomedical Center, P.O. Box 571, SE-751 23 Uppsala, Sweden. Mattias.Gareskog@medcellbiol.uu.se
Abstract:
It has been suggested that protein kinase C (PKC) is involved in the etiology of diabetic complications. The aim of the present study was to investigate the putative involvement of different PKC isoforms (alpha, beta1, beta 2, gamma, delta, epsilon, and zeta) in the embryopathy of diabetic rat pregnancy. Embryos were collected from normal and diabetic rats and assayed for PKC activity, PKC mRNA levels, and PKC protein distribution on gestational d 10 and 11. Embryos of diabetic rats showed markers of increased activity of PKC-alpha, PKC-beta1, PKC-gamma, PKC-delta, and PKC-zeta compared with embryos of normal rats on d 10. In addition, the malformed embryos had further increased PKC-gamma, and PKC-delta activity markers compared with nonmalformed embryos of diabetic rats on gestational d 10. In contrast, maternal diabetes caused only two alterations in PKC activity markers on gestational d 11, i.e. both PKC-alpha and PKC-zeta were decreased in embryos of diabetic rats. We found increased mRNA levels of PKC-beta 1 and PKC-zeta on d 10 in embryos of diabetic rats and decreased mRNA levels of PKC-gamma on d 11 in embryos of diabetic rats. Malformed embryos from diabetic rats showed increased distribution of PKC-beta 1 and PKC-beta 2 protein in the tissue compared with nonmalformed embryos from diabetic rats and embryos from normal rats. We conclude that diabetic rat embryopathy may be associated with increased activity and enhanced tissue distribution of several PKC isoforms in early organogenesis.
Insights
Diabetic embryopathy in rats is linked to altered protein kinase C (PKC) activity and distribution. Specific PKC isoforms show increased activity and tissue presence in embryos from diabetic mothers, particularly during early organogenesis.
Area of Science:
- Biochemistry
- Developmental Biology
- Endocrinology
Background:
- Protein kinase C (PKC) involvement in diabetic complications is suggested.
- Diabetic embryopathy is a known complication of poorly controlled diabetes during pregnancy.
Purpose of the Study:
- To investigate the role of various protein kinase C (PKC) isoforms (alpha, beta1, beta2, gamma, delta, epsilon, zeta) in diabetic rat embryopathy.
- To assess PKC activity, mRNA levels, and protein distribution in embryos from diabetic and normal pregnancies.
Main Methods:
- Embryos were collected from normal and diabetic rats on gestational days 10 and 11.
- Assays for PKC activity, PKC mRNA levels, and PKC protein distribution were performed.
- Comparison between embryos from diabetic vs. normal rats, and malformed vs. non-malformed embryos from diabetic rats.
Main Results:
- Increased activity of PKC-alpha, -beta1, -gamma, -delta, and -zeta was observed in embryos from diabetic rats on day 10.
- Malformed embryos showed further increased PKC-gamma and -delta activity.
- Increased mRNA levels of PKC-beta1 and -zeta on day 10, and decreased PKC-gamma mRNA on day 11 were noted.
- Enhanced tissue distribution of PKC-beta1 and -beta2 protein was found in malformed embryos.
Conclusions:
- Diabetic rat embryopathy is associated with altered activity of multiple PKC isoforms during early organogenesis.
- Increased activity and tissue distribution of specific PKC isoforms may contribute to the development of diabetic embryopathy.
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