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Angiotensin-(1-7) Abrogates Mitogen-Stimulated Proliferation of Cardiac Fibroblasts

Content Provider	PubMed Central
Author	Mccollum, Latronya T. Gallagher, Patricia E. Tallant, E. Ann
Copyright Year	2012
Abstract	Previous studies showed that angiotensin-(1-7) [Ang-(1-7)] attenuates cardiac remodeling by reducing both interstitial and perivascular fibrosis. Although a high affinity binding site for Ang-(1-7) was identified on cardiac fibroblasts, the molecular mechanisms activated by the heptapeptide hormone were not identified. We isolated cardiac fibroblasts from neonatal rat hearts to investigate signaling pathways activated by Ang-(1-7) that participate in fibroblast proliferation. Ang-(1-7) reduced 3H-thymidine, -leucine and –proline incorporation into cardiac fibroblasts stimulated with serum or the mitogen endothelin-1 (ET-1), demonstrating that the heptapeptide hormone decreases DNA, protein and collagen synthesis. The reduction in DNA synthesis by Ang-(1-7) was blocked by the AT(1-7) receptor antagonist [D-Ala7]-Ang-(1-7), showing specificity of the response. Treatment of cardiac fibroblasts with Ang-(1-7) reduced the Ang II- or ET-1-stimulated increase in phospho-ERK1 and –ERK2. In contrast, Ang-(1-7) increased dual-specificity phosphatase DUSP1 immunoreactivity and mRNA, suggesting that the heptapeptide hormone increases DUSP1 to reduce MAP kinase phosphorylation and activity. Incubation of cardiac fibroblasts with ET-1 increased cyclooxygenase 2 (COX-2) and prostaglandin synthase (PGES) mRNAs, while Ang-(1-7) blocked the increase in both enzymes, suggesting that the heptapeptide hormone alters the concentration and the balance between the proliferative and anti-proliferative prostaglandins. Collectively, these results indicate that Ang-(1-7) participates in maintaining cardiac homeostasis by reducing proliferation and collagen production by cardiac fibroblasts in association with up-regulation of DUSP1 to reduce MAP kinase activities and attenuation of the synthesis of mitogenic prostaglandins. Increased Ang-(1-7) or agents that enhance production of the heptapeptide hormone may prevent abnormal fibrosis that occurs during cardiac pathologies.
Related Links	http://dx.doi.org/10.1016/j.peptides.2012.01.020
Ending Page	388
Page Count	9
Starting Page	380
File Format	PDF
ISSN	01969781
e-ISSN	18735169
Journal	Peptides
Issue Number	2
Volume Number	34
Language	English
Publisher Date	2012-04-01
Access Restriction	Open
Subject Keyword	Biochemistry Physiology Endocrinology Cellular and Molecular Neuroscience Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Physiology Biochemistry Cellular and Molecular Neuroscience Endocrinology

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