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Cultured myofibroblasts generate angiotensin peptides de novo.
J Mol Cell Cardiol. 1997 May; 29(5):1375-86.JM

Abstract

Scar tissue found at the site of myocardial infarction (MI) contains phenotypically transformed fibroblast-like cells termed myofibroblasts (myoFb). In injured cardiac tissue, autoradiography and immunolabeling have localized high density angiotensin (Ang) converting enzyme (ACE) and Ang II receptor binding to these cells, suggesting that they may regulate local concentrations of Ang II and transduce signals at this site. Ang II is known to modulate type I collagen gene expression of fibroblasts and myoFb, and to promote fibrous tissue contraction, each of which may contribute to tissue repair. It is unknown whether myoFb themselves generate Ang peptides de novo via expression of angiotensinogen (Ao), an aspartyl protease needed to convert Ao to Ang I, and ACE. We therefore isolated and cultured myoFb from 4-week-old scar tissue of the adult rat left ventricle with transmural MI. In cultured myoFb we found: (a) immunoreactive membrane-bound ACE, cytosolic cathepsin D (Cat-D), and AT, receptors by immunofluorescence and confocal microscopy, (b) mRNA expression for Ao, ACE, and Cat-D, but not renin, by reverse transcriptase-polymerase chain reaction, (c) production of Ang I and II in serum-free culture media; (d) absence of renin activity; (e) a time-dependent conversion of Ao to Ang I by myoFb cytosol, which was inhibited by pepstatin A, but not by renin inhibitor; and (f) significant increase in Ang II production (P < 0.05) by exogenous Ao and Ang I (10 nM), which was significantly blocked by lisinopril (0.1 microM: P < 0.05). Thus, cultured myoFb express requisite components and are able to generate Ang I and II de novo. In an autocrine and/or paracrine manner, Ang II may regulate myoFb collagen turnover and fibrous tissue contraction.

Authors+Show Affiliations

Department of Internal Medicine, University of Missouri Health Sciences Center, Columbia 65212, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

9201623

Citation

Katwa, L C., et al. "Cultured Myofibroblasts Generate Angiotensin Peptides De Novo." Journal of Molecular and Cellular Cardiology, vol. 29, no. 5, 1997, pp. 1375-86.
Katwa LC, Campbell SE, Tyagi SC, et al. Cultured myofibroblasts generate angiotensin peptides de novo. J Mol Cell Cardiol. 1997;29(5):1375-86.
Katwa, L. C., Campbell, S. E., Tyagi, S. C., Lee, S. J., Cicila, G. T., & Weber, K. T. (1997). Cultured myofibroblasts generate angiotensin peptides de novo. Journal of Molecular and Cellular Cardiology, 29(5), 1375-86.
Katwa LC, et al. Cultured Myofibroblasts Generate Angiotensin Peptides De Novo. J Mol Cell Cardiol. 1997;29(5):1375-86. PubMed PMID: 9201623.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Cultured myofibroblasts generate angiotensin peptides de novo. AU - Katwa,L C, AU - Campbell,S E, AU - Tyagi,S C, AU - Lee,S J, AU - Cicila,G T, AU - Weber,K T, PY - 1997/5/1/pubmed PY - 1997/5/1/medline PY - 1997/5/1/entrez SP - 1375 EP - 86 JF - Journal of molecular and cellular cardiology JO - J Mol Cell Cardiol VL - 29 IS - 5 N2 - Scar tissue found at the site of myocardial infarction (MI) contains phenotypically transformed fibroblast-like cells termed myofibroblasts (myoFb). In injured cardiac tissue, autoradiography and immunolabeling have localized high density angiotensin (Ang) converting enzyme (ACE) and Ang II receptor binding to these cells, suggesting that they may regulate local concentrations of Ang II and transduce signals at this site. Ang II is known to modulate type I collagen gene expression of fibroblasts and myoFb, and to promote fibrous tissue contraction, each of which may contribute to tissue repair. It is unknown whether myoFb themselves generate Ang peptides de novo via expression of angiotensinogen (Ao), an aspartyl protease needed to convert Ao to Ang I, and ACE. We therefore isolated and cultured myoFb from 4-week-old scar tissue of the adult rat left ventricle with transmural MI. In cultured myoFb we found: (a) immunoreactive membrane-bound ACE, cytosolic cathepsin D (Cat-D), and AT, receptors by immunofluorescence and confocal microscopy, (b) mRNA expression for Ao, ACE, and Cat-D, but not renin, by reverse transcriptase-polymerase chain reaction, (c) production of Ang I and II in serum-free culture media; (d) absence of renin activity; (e) a time-dependent conversion of Ao to Ang I by myoFb cytosol, which was inhibited by pepstatin A, but not by renin inhibitor; and (f) significant increase in Ang II production (P < 0.05) by exogenous Ao and Ang I (10 nM), which was significantly blocked by lisinopril (0.1 microM: P < 0.05). Thus, cultured myoFb express requisite components and are able to generate Ang I and II de novo. In an autocrine and/or paracrine manner, Ang II may regulate myoFb collagen turnover and fibrous tissue contraction. SN - 0022-2828 UR - https://www.unboundmedicine.com/medline/citation/9201623/Cultured_myofibroblasts_generate_angiotensin_peptides_de_novo_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0022-2828(97)90376-X DB - PRIME DP - Unbound Medicine ER -