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Pouch tissue and angiotensin peptide generation.
J Mol Cell Cardiol. 1998 Jul; 30(7):1401-13.JM

Abstract

Myofibroblasts and their potential to generate angiotensin (Ang) II and transforming growth factor beta 1 (TGF-beta 1) at sites of infarction in the rat heart have been implicated in tissue repair. These cells likewise contribute to repair in a subcutaneous pouch model of fibrous tissue formation. Their appearance in pouch tissue coincides with high density ACE and Ang II receptor binding, suggesting a role for Ang II in tissue repair. Using pouch tissue studied at different time points of repair, the present study examined the expression of requisite mRNA for Ang peptide generation: angiotensinogen, Ao; an aspartyl protease, either cathepsin-D, Cat-D, or renin: and angiotensin converting enzyme, ACE, TGF-beta 1 and type I collagen mRNA expression was also addressed. Unlike pouch studied on day 2 and 4, at 7, 14 and 21 days, we found: (a) expression of Ao, Cat-D but not renin, ACE and TGF-beta 1 mRNA; (b) Ang I and Ang II peptides in pouch tissue and exudate; (c) the presence of Cat-D activity but no renin activity; (d) an increase in type I collagen mRNA with time; (e) upregulation of pouch tissue ACE mRNA expression by lisinopril treatment, whereas AT1 and AT2 receptor antagonists (losartan and PD 123177, respectively) downregulated the expression of mRNA for ACE, when compared to untreated controls; (f) downregulation of TGF-beta 1 mRNA expression by lisinopril and losartan compared to untreated controls; and (g) PD 123177 had no effect, whereas lisinopril and losartan treatment significantly (P < 0.05) reduced type I collagen mRNA expression. Thus, in this model of fibrous tissue formation, we found expression of component genes involved in Ang peptide (I and II) and TGF-beta 1 generation and Ang II upregulation of TGF-beta 1 expression, suggesting Ang II and/or TGF-beta 1 may upregulate type I collagen expression during tissue repair. Pharmacologic intervention studies with lisinopril or losartan indicate Ang II plays a role in the reciprocal regulation of ACE mRNA expression, which modulates Ang II levels at sites of repair.

Authors+Show Affiliations

Department of Internal Medicine, Dalton Cardiovascular Research Center, Columbia, MO, USA.No affiliation info availableNo 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

9710808

Citation

Katwa, L C., et al. "Pouch Tissue and Angiotensin Peptide Generation." Journal of Molecular and Cellular Cardiology, vol. 30, no. 7, 1998, pp. 1401-13.
Katwa LC, Sun Y, Campbell SE, et al. Pouch tissue and angiotensin peptide generation. J Mol Cell Cardiol. 1998;30(7):1401-13.
Katwa, L. C., Sun, Y., Campbell, S. E., Tyagi, S. C., Dhalla, A. K., Kandala, J. C., & Weber, K. T. (1998). Pouch tissue and angiotensin peptide generation. Journal of Molecular and Cellular Cardiology, 30(7), 1401-13.
Katwa LC, et al. Pouch Tissue and Angiotensin Peptide Generation. J Mol Cell Cardiol. 1998;30(7):1401-13. PubMed PMID: 9710808.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Pouch tissue and angiotensin peptide generation. AU - Katwa,L C, AU - Sun,Y, AU - Campbell,S E, AU - Tyagi,S C, AU - Dhalla,A K, AU - Kandala,J C, AU - Weber,K T, PY - 1998/8/26/pubmed PY - 1998/8/26/medline PY - 1998/8/26/entrez SP - 1401 EP - 13 JF - Journal of molecular and cellular cardiology JO - J. Mol. Cell. Cardiol. VL - 30 IS - 7 N2 - Myofibroblasts and their potential to generate angiotensin (Ang) II and transforming growth factor beta 1 (TGF-beta 1) at sites of infarction in the rat heart have been implicated in tissue repair. These cells likewise contribute to repair in a subcutaneous pouch model of fibrous tissue formation. Their appearance in pouch tissue coincides with high density ACE and Ang II receptor binding, suggesting a role for Ang II in tissue repair. Using pouch tissue studied at different time points of repair, the present study examined the expression of requisite mRNA for Ang peptide generation: angiotensinogen, Ao; an aspartyl protease, either cathepsin-D, Cat-D, or renin: and angiotensin converting enzyme, ACE, TGF-beta 1 and type I collagen mRNA expression was also addressed. Unlike pouch studied on day 2 and 4, at 7, 14 and 21 days, we found: (a) expression of Ao, Cat-D but not renin, ACE and TGF-beta 1 mRNA; (b) Ang I and Ang II peptides in pouch tissue and exudate; (c) the presence of Cat-D activity but no renin activity; (d) an increase in type I collagen mRNA with time; (e) upregulation of pouch tissue ACE mRNA expression by lisinopril treatment, whereas AT1 and AT2 receptor antagonists (losartan and PD 123177, respectively) downregulated the expression of mRNA for ACE, when compared to untreated controls; (f) downregulation of TGF-beta 1 mRNA expression by lisinopril and losartan compared to untreated controls; and (g) PD 123177 had no effect, whereas lisinopril and losartan treatment significantly (P < 0.05) reduced type I collagen mRNA expression. Thus, in this model of fibrous tissue formation, we found expression of component genes involved in Ang peptide (I and II) and TGF-beta 1 generation and Ang II upregulation of TGF-beta 1 expression, suggesting Ang II and/or TGF-beta 1 may upregulate type I collagen expression during tissue repair. Pharmacologic intervention studies with lisinopril or losartan indicate Ang II plays a role in the reciprocal regulation of ACE mRNA expression, which modulates Ang II levels at sites of repair. SN - 0022-2828 UR - https://www.unboundmedicine.com/medline/citation/9710808/Pouch_tissue_and_angiotensin_peptide_generation_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0022-2828(98)90708-8 DB - PRIME DP - Unbound Medicine ER -