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See Latest ArticlesDominant negative p38 mitogen-activated protein kinase prevents cardiac apoptosis and remodeling after streptozotocin-induced diabetes mellitus
Heart And Circulatory Physiology, 07/21/09
Thandavarayan RA et al. – Data establish that p38 mitogen-activated protein kinase (MAPK) activity is required for cardiac remodeling after diabetes induction and suggest that p38{alpha} MAPK may promote cardiomyocyte apoptosis by down-regulation of Bcl-XL.
Methods- Study of role of p38{alpha} MAPK after experimental diabetes
- Use of transgenic mice with cardiac-specific expression of a dominant-negative mutant form of p38{alpha} MAPK (TG)
- Comparable elevation of blood glucose between nontransgenic (NTG) and TG mice
- Expression of phospho-p38 MAPK and phospho-MAPKAPK-2 levels significantly suppressed in TG mice heart than in NTG mice after diabetes induction
- Smaller left ventricular (LV) dimension in systole and higher percent fractional shortening in diabetic TG mice vs diabetic NTG mice
- Reduced cardiac myocyte diameter, content of cardiac fibrosis, LV tissue expressions of atrial natriuretic peptide, transforming growth factor {beta}1, and collagen III in diabetic TG mice vs diabetic NTG mice
- LV expression of NADPH oxidase subunits, p22 phox, p67 phox, gp91 phox and Nox4, reactive oxygen species and lipid peroxidation levels significantly increased in diabetic NTG mice vs diabetic TG mice
- Less myocardial apoptosis, number of caspase-3 positive cells and down-regulation of anti-apoptotic protein Bcl-XL in diabetic TG mice vs diabetic NTG mice
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