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Protection from Diabetes‐Associated Apoptosis with Heat Shock Protein 27 Overexpression
Author(s) -
Williamson Courtney L,
Dabkowski Erinne R,
Brock Robert W,
Frisbee Jefferson C,
Hollander John M
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.953.18
Subject(s) - hsp27 , medicine , diabetic cardiomyopathy , endocrinology , heat shock protein , apoptosis , diabetes mellitus , hsp70 , streptozotocin , cardiac function curve , biology , cardiomyopathy , heart failure , biochemistry , gene
Diabetic cardiomyopathy is associated with cardiac contractile abnormalities which may result from and enhanced apoptotic susceptibility. The small heat shock protein 27 (hsp27) contributes to preservation of cytoskeletal structure which may impact the apoptotic program. The goal of this study was to determine whether hsp27 overexpression influences diabetes‐induced apoptosis. Transgenic mice overexpressing hsp27 and littermate controls were made diabetic by streptozotocin injection and sacrificed seven weeks following diabetic onset. Hsp27 overexpression preserved cardiac contractile function in the diabetic heart as indicated by enhanced rates of relaxation and contraction, as well as developed pressures ( P <0.05 for all three). Caspase activity was decreased in diabetic hearts overexpressing hsp27 as compared to diabetic littermate controls ( P <0.05). Cytochrome c and apoptosis‐inducing factor content in the cytosolic fraction was decreased in diabetic hearts overexpressing hsp27 as compared to diabetic littermate controls ( P <0.05 for both). There was an increased association of hsp27 and alpha‐actin in diabetic hearts overexpressing hsp27 as compared to diabetic littermate controls. These results suggest that hsp27 overexpression attenuates cardiac contractile abnormalities resulting from diabetic insult, which is associated with a decrease in apoptosis susceptibility.