Autor: | Kazuo Komamura, Toshiyuki Miyata, Kunio Miyatake, Kenji Sunagawa, Masafumi Kitakaze, Rie Tatsumi, Hiroko Shirotani-Ikejima, Yuko Tsujita-Kuroda |
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Rok vydání: | 2003 |
Předmět: |
Pharmacology
medicine.medical_specialty biology business.industry Skeletal muscle General Medicine medicine.disease Prostaglandin-D synthase Muscle hypertrophy Gastrocnemius muscle Atrophy medicine.anatomical_structure Endocrinology Internal medicine biology.protein Medicine Pharmacology (medical) medicine.symptom Cardiology and Cardiovascular Medicine business Myopathy Dexamethasone Glucocorticoid medicine.drug |
Zdroj: | Cardiovascular Drugs and Therapy. 17:303-310 |
ISSN: | 0920-3206 |
DOI: | 10.1023/a:1027352703783 |
Popis: | Administration of glucocorticoids results in hypertension, cardiac hypertrophy, and general myopathy. The present study analyzed the acute effect of dexamethasone (0.5 mg/100 g for 3 days) or dexamethasone plus insulin-like growth factor-1 (0.35 mg/100 g for 3 days) on differential gene expression in the gastrocnemius muscle and the left ventricular myocardium of rats. Dexamethasone induced atrophy of gastrocnemius muscle. Cathepsin L, and not ubiquitin, was the earliest mediator of skeletal muscle proteolysis induced by dexamethasone. Insulin-like growth factor-1 reversed gastrocnemius muscle mass, and deleted a part of downregulated genes by dexamethasone. On the other hand, dexamethasone administration did not result in cardiac hypertrophy or hypertension. Only prostaglandin D synthase gene was upregulated by dexamethasone in myocardium, and genes related to extracellular matrix and proteinase inhibitor were downregulated. Molecular alteration for hypertrophy might have initiated. Dexamethasone-induced proteolysis and reversal with insulin-like growth factor-1 occurred rapidly in skeletal muscle; but was relatively delayed in the myocardium. |
Databáze: | OpenAIRE |
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