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Renin expression at sites of repair in the infarcted rat heart.
J Mol Cell Cardiol. 2001 May; 33(5):995-1003.JM

Abstract

Y. Sun, J. Zhang, J. Q. Zhang and K. T. Weber. Renin Expression at Sites of Repair in the Infarcted Rat Heart. Journal of Molecular and Cellular Cardiology (2001) 33, 995-1003. Angiotensin (Ang) II has autocrine and paracrine functions that contribute to structural cardiac remodeling by fibrous tissue following myocardial infarction (MI). The recruitment of angiotensin converting enzyme (ACE) and AngII receptors by inflammatory and fibroblast-like cells involved in tissue repair of the infarcted heart is now well established. On the other hand, the temporal and spatial response and cellular source of renin in infarcted hearts have not been fully elucidated. The relationship between renin synthesis and circulating renin activity have likewise not been addressed. The present study sought to assess the cellular source, spatial distribution and temporal response of renin expression and synthesis in the rat heart following anterior transmural MI, and to determine its relationship to circulating renin activity. At day 3 and weeks 1, 2, 3 and 4 following left coronary artery ligation, the localization and optical density of cardiac renin mRNA was detected by quantitative in situ hybridization; cardiac and circulating renin activity was measured by radioimmunoassay; cells expressing cardiac renin were detected by immunohistochemistry; and injury/repair was assessed by hematoxylin/eosin and collagen-specific picrosirius red staining. Unoperated rats served as normal controls. The authors found: (1) renin mRNA and activity were not detected in either normal control or non-infarcted myocardium, but were expressed at the site of infarction and other sites of repair involving visceral pericardium and endocardium of interventricular septum at all time points; (2) cells expressing renin at day 3 and weeks 1 and 2 were predominantly macrophages, while at weeks 3 and 4, they were primarily myofibroblasts; (3) renin activity in the infarcted myocardium rose progressively over the course of 4 weeks; and (4) circulating renin activity was significantly increased at day 3 and week 1, reached a peak at week 2, declined at week 3 and returned to normal levels at week 4. Thus, renin expression and activity appear at sites of repair in the infarcted rat heart on day 3 and rise progressively thereafter over 4 weeks, independent of circulating renin. Several types of cells are responsible for renin synthesis at these sites; primarily macrophages during the inflammatory phase of repair, and myofibroblasts during the subsequent fibrogenic phase. Cardiac renin production following MI contributes to local AngII generation that regulates tissue repair and structural remodeling following MI.

Authors+Show Affiliations

Division of Cardiovascular Diseases, Department of Medicine, Unuiversity of Tennessee Health Science Center, 956 Court Avenue, Memphis, TN 38163, USA. yasun@utmem.eduNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

11343421

Citation

Sun, Y, et al. "Renin Expression at Sites of Repair in the Infarcted Rat Heart." Journal of Molecular and Cellular Cardiology, vol. 33, no. 5, 2001, pp. 995-1003.
Sun Y, Zhang J, Zhang JQ, et al. Renin expression at sites of repair in the infarcted rat heart. J Mol Cell Cardiol. 2001;33(5):995-1003.
Sun, Y., Zhang, J., Zhang, J. Q., & Weber, K. T. (2001). Renin expression at sites of repair in the infarcted rat heart. Journal of Molecular and Cellular Cardiology, 33(5), 995-1003.
Sun Y, et al. Renin Expression at Sites of Repair in the Infarcted Rat Heart. J Mol Cell Cardiol. 2001;33(5):995-1003. PubMed PMID: 11343421.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Renin expression at sites of repair in the infarcted rat heart. AU - Sun,Y, AU - Zhang,J, AU - Zhang,J Q, AU - Weber,K T, PY - 2001/5/10/pubmed PY - 2001/7/20/medline PY - 2001/5/10/entrez SP - 995 EP - 1003 JF - Journal of molecular and cellular cardiology JO - J Mol Cell Cardiol VL - 33 IS - 5 N2 - Y. Sun, J. Zhang, J. Q. Zhang and K. T. Weber. Renin Expression at Sites of Repair in the Infarcted Rat Heart. Journal of Molecular and Cellular Cardiology (2001) 33, 995-1003. Angiotensin (Ang) II has autocrine and paracrine functions that contribute to structural cardiac remodeling by fibrous tissue following myocardial infarction (MI). The recruitment of angiotensin converting enzyme (ACE) and AngII receptors by inflammatory and fibroblast-like cells involved in tissue repair of the infarcted heart is now well established. On the other hand, the temporal and spatial response and cellular source of renin in infarcted hearts have not been fully elucidated. The relationship between renin synthesis and circulating renin activity have likewise not been addressed. The present study sought to assess the cellular source, spatial distribution and temporal response of renin expression and synthesis in the rat heart following anterior transmural MI, and to determine its relationship to circulating renin activity. At day 3 and weeks 1, 2, 3 and 4 following left coronary artery ligation, the localization and optical density of cardiac renin mRNA was detected by quantitative in situ hybridization; cardiac and circulating renin activity was measured by radioimmunoassay; cells expressing cardiac renin were detected by immunohistochemistry; and injury/repair was assessed by hematoxylin/eosin and collagen-specific picrosirius red staining. Unoperated rats served as normal controls. The authors found: (1) renin mRNA and activity were not detected in either normal control or non-infarcted myocardium, but were expressed at the site of infarction and other sites of repair involving visceral pericardium and endocardium of interventricular septum at all time points; (2) cells expressing renin at day 3 and weeks 1 and 2 were predominantly macrophages, while at weeks 3 and 4, they were primarily myofibroblasts; (3) renin activity in the infarcted myocardium rose progressively over the course of 4 weeks; and (4) circulating renin activity was significantly increased at day 3 and week 1, reached a peak at week 2, declined at week 3 and returned to normal levels at week 4. Thus, renin expression and activity appear at sites of repair in the infarcted rat heart on day 3 and rise progressively thereafter over 4 weeks, independent of circulating renin. Several types of cells are responsible for renin synthesis at these sites; primarily macrophages during the inflammatory phase of repair, and myofibroblasts during the subsequent fibrogenic phase. Cardiac renin production following MI contributes to local AngII generation that regulates tissue repair and structural remodeling following MI. SN - 0022-2828 UR - https://www.unboundmedicine.com/medline/citation/11343421/Renin_expression_at_sites_of_repair_in_the_infarcted_rat_heart_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0022-2828(01)91365-3 DB - PRIME DP - Unbound Medicine ER -