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1 Laboratory of Cardiovascular Science, NIH, National Institute on Aging, Baltimore, MD, USA; Division of Cellular and Molecular Cardiology, Sree Chitra Tirunal Institute for Medical Science and Technology, Trivandrum, India, India
2 The Cardiovascular Research Institute, Texas A & M University System Health Science Center, Temple, TX, USA
3 Laboratory of Cardiovascular Science, NIH, National Institute on Aging, Baltimore, MD, USA
* To whom correspondence should be addressed. E-mail: shivak{at}sctimst.ker.nic.in.
The intracardiac angiotensin II-forming pathway is activated in the senescent myocardium, raising the possibility of enhanced angiotensin II effects on cardiac fibroblasts. This study established an in vitro model of cultured cardiac fibroblasts from aged rats to examine if the response of these cells to angiotensin II is modified in the aged heart. Levels of mRNA encoding renin, angiotensinogen and the AT1 receptor subtype in cardiac fibroblasts from young adult and senescent rats were quantified by reverse transcriptase-polymerase chain reaction, net collagen production by a hydroxyproline-based assay and TGF-
levels using a commercial kit. In cardiac fibroblasts from young adult rats, angiotensin II significantly enhanced AT1 mRNA levels, net collagen production and TGF- production. In fibroblasts from the aged myocardium, angiotensin II down-regulated AT1 mRNA expression, had a less pronounced effect on net collagen production and had no effect on TGF- production. Such age-related modification of the response of cardiac fibroblasts to angiotensin II may counteract the effects of augmented intracardiac angiotensin II production in the senescent heart, limiting fibrogenesis.
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