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The Effects of Autophagy on Diabetic Cardiomyopathy
Author(s) -
Kim JooHeon,
Lee Youngjeon,
Hong Yunkyung,
Kim Sunmi,
Hong Yonggeun
Publication year - 2011
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.25.1_supplement.1095.2
Subject(s) - autophagy , diabetic cardiomyopathy , cardiomyopathy , cardiology , medicine , chemistry , heart failure , biochemistry , apoptosis
Diabetes is a major predictor of heart failure. However, little is known regarding mechanisms how it causes cardiomyopathy. The purpose of this study was to determine whether prolonged exposure of cardiomyocytes to high glucose concentrations induces autophagy. For in vitr o study, H9c2 cells were cultured with high glucose for 3 days. Cell viability was determined by trypan blue assay. Autophagic vacuoles were detected by MDC staining as well as immunoblot. For in vivo study, diabetes mellitus was induced by streptozotocin, 60mg/kg of body weight, intraperitoneally at 4‐week‐age in SD rats. Body weight and blood glucose level were monitored and sacrificed at 2 and 5 weeks. Deprived glucose as well as high glucose within medium induced a significant decrease of cell viability at 72hr. The conversion ratio of LC3 was significantly increased by high glucose at the same time. However, glucose deprivation dramatically converts LC3| to LC3|| at 12hr. Diabetic rats have shown the reduction of size of LV with growth retardation (p<.05) and higher level of LC3 protein expression, suggesting that autophagy was activated. Taken together, in vitro findings indicate that hyperglycemic oxidative stress is inducible to autophagy. In vivo studies show progression of pathological remodeling of heart development is associated with autophagy. Thereby, there might be potential role of autophagy in pathogenesis of diabetic cardimyocytes.