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Your search keyword '"Isshiki, Keiji"' showing total 14 results
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14 results on '"Isshiki, Keiji"'

13. Long-Term PKC Inhibition with Oral Administration of PKC [Beta] Inhibitor Prevents Diabetic Glomerular Pathologies

Author

KOYA, DAISUKE, HANEDA, MASAKAZU, NAKAGAWA, HIROKO, ISSHIKI, KEIJI, SATO, HARUHISA, and KIKKAWA, RYUICHI

Subjects
Diabetic nephropathies -- Care and treatment, Hypoglycemic agents -- Physiological aspects, Chronic kidney failure -- Prevention, Health
Abstract

Diabetic nephropathy is the leading cause of end-stage renal disease (ESRD) in Western and Asian society. We have previously shown that short-term treatment of streptozotocin-induced diabetic rats with PKC [Beta] [...]

Published
2000

14. Expression of connective tissue growth factor is increased in injured myocardium associated with protein kinase C beta2 activation and diabetes.

Author

Way, Kerrie J., Isshiki, Keiji, Suzuma, Kiyoshi, Yokota, Tamotsu, Zvagelsky, Dmitriy, Schoen, Frederick J., Sandusky, George E., Pechous, Penelope A., Vlahos, Chris J., Wakasaki, Hisao, and King, George L.

Subjects
*GROWTH factors, *CONNECTIVE tissues, *HEART fibrosis, *HEART metabolism, *PROTEIN metabolism, *ANIMAL experimentation, *BIOCHEMISTRY, *COMPARATIVE studies, *DIABETES, *EXTRACELLULAR space, *HEART ventricles, *IMMUNOLOGY technique, *ISOENZYMES, *PHENOMENOLOGY, *RESEARCH methodology, *MEDICAL cooperation, *MICE, *MYOCARDIUM, *CARDIOMYOPATHIES, *PROTEIN kinases, *RATS, *RESEARCH, *STAINS & staining (Microscopy), *TRANSFERASES, *EVALUATION research, *FIBROSIS, *CONNECTIVE tissue growth factor
Abstract

Protein kinase C (PKC) beta isoform activity is increased in myocardium of diabetic rodents and heart failure patients. Transgenic mice overexpressing PKCbeta2 (PKCbeta2Tg) in the myocardium exhibit cardiomyopathy and cardiac fibrosis. In this study, we characterized the expression of connective tissue growth factor (CTGF) and transforming growth factor beta (TGFbeta) with the development of fibrosis in heart from PKCbeta2Tg mice at 4-16 weeks of age. Heart-to-body weight ratios of transgenic mice increased at 8 and 12 weeks, indicating hypertrophy, and ratios did not differ at 16 weeks. Collagen VI and fibronectin mRNA expression increased in PKCbeta2Tg hearts at 4-12 weeks. Histological examination revealed myocyte hypertrophy and fibrosis in 4- to 16-week PKCbeta2Tg hearts. CTGF expression increased in PKCbeta2Tg hearts at all ages, whereas TGFbeta increased only at 8 and 12 weeks. In 8-week diabetic mouse heart, CTGF and TGFbeta expression increased two- and fourfold, respectively. Similarly, CTGF expression increased in rat hearts at 2-8 weeks of diabetes. This is the first report of increased CTGF expression in myocardium of diabetic rodents suggesting that cardiac injury associated with PKCbeta2 activation, diabetes, or heart failure is marked by increased CTGF expression. CTGF could act independently or together with other cytokines to induce cardiac fibrosis and dysfunction. [ABSTRACT FROM AUTHOR]

Published
2002
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