We have located links that may give you full text access.
JOURNAL ARTICLE
RESEARCH SUPPORT, NON-U.S. GOV'T
All-trans retinoic acid inhibited angiotensin II-induced increase in cell growth and collagen secretion of neonatal cardiac fibroblasts.
Acta Pharmacologica Sinica 2006 April
AIM: To determine whether all-trans retinoic acid (atRA) acts to modulate angiotensin II (Ang II)-induced cardiac fibroblast cell growth and collagen secretion.
METHODS: Cultured neonatal rat cardiac fibroblasts (CF) were used in the experiment. A 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay was used to detect cell growth of the CF; and immunocytochemistry and Western blotting were used to measure the production and secretion of collagen and the expression of transforming growth factor-beta1 (TGF-beta1) by the CF.
RESULTS: atRA (10(-7) to 10(-5) mol/L) inhibited the Ang II-induced increase in cell growth of CF (P<0.05). Ang II stimulated the secretion of collagen types I and III by the CF. This effect was blocked by AT(1) receptor antagonist losartan (10(-6) mol/L), but not by AT2 receptor antagonist PD123319 (up to 10(-6) mol/L). Exposure of CF to atRA (10(-5) mol/L) attenuated the Ang II-induced increase in the secretion of collagen types I and III (P<0.05). atRA (10(-5) mol/L) also blocked the Ang II-induced increase in the expression of TGF-beta1.
CONCLUSION: atRA inhibits the Ang II-induced increase in cell growth and collagen secretion of neonatal rat CF. The effect of atRA is possibly mediated by lowering the TGF-beta1 level. These observations support the notion that atRA is a potential candidate for the prevention and therapy of cardiac remodeling.
METHODS: Cultured neonatal rat cardiac fibroblasts (CF) were used in the experiment. A 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay was used to detect cell growth of the CF; and immunocytochemistry and Western blotting were used to measure the production and secretion of collagen and the expression of transforming growth factor-beta1 (TGF-beta1) by the CF.
RESULTS: atRA (10(-7) to 10(-5) mol/L) inhibited the Ang II-induced increase in cell growth of CF (P<0.05). Ang II stimulated the secretion of collagen types I and III by the CF. This effect was blocked by AT(1) receptor antagonist losartan (10(-6) mol/L), but not by AT2 receptor antagonist PD123319 (up to 10(-6) mol/L). Exposure of CF to atRA (10(-5) mol/L) attenuated the Ang II-induced increase in the secretion of collagen types I and III (P<0.05). atRA (10(-5) mol/L) also blocked the Ang II-induced increase in the expression of TGF-beta1.
CONCLUSION: atRA inhibits the Ang II-induced increase in cell growth and collagen secretion of neonatal rat CF. The effect of atRA is possibly mediated by lowering the TGF-beta1 level. These observations support the notion that atRA is a potential candidate for the prevention and therapy of cardiac remodeling.
Full text links
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app
All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.
By using this service, you agree to our terms of use and privacy policy.
Your Privacy Choices
You can now claim free CME credits for this literature searchClaim now
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app