کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
1938466 | 1050740 | 2007 | 6 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Involvement of c-Jun N-terminal kinases activation in diabetic embryopathy
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موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
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چکیده انگلیسی
The mechanisms for diabetic embryopathy are not well understood. JNK1/2 activation is increased in diabetic embryopathy, and antioxidants abolish JNK activation, and thus, ameliorate diabetic embryopathy. Phosphorylated SEK1 were significantly elevated in malformed embryos from diabetic mouse. In a dose-dependent manner, JNK inhibitor (SP600125) significantly reduced hyperglycemia-induced embryopathy. Malformation rates in embryos from the diabetic WT group were 15.6-fold higher than that in the non-diabetic WT control group. Jnk2 null mutant (JNKKO mice) was associated with a 71% reduction in the malformation rate of embryos under maternal diabetic conditions. Embryos cultured in 0.5Â mM sorbitol (JNK activator) had a malformation rate that was significantly higher than that of the control group. Pharmacological and genetic evidence from the present studies strongly support JNK activation being an indispensable mediator of diabetic embryopathy. JNK activation itself is sufficient to induce embryonic anomalies, and thus mimics the teratogenic effect of hyperglycemia.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 357, Issue 3, 8 June 2007, Pages 749-754
Journal: Biochemical and Biophysical Research Communications - Volume 357, Issue 3, 8 June 2007, Pages 749-754
نویسندگان
Peixin Yang, Zhiyong Zhao, E. Albert Reece,