Deficient prolylcarboxypeptidase gene and protein expression in left ventricles of spontaneously hypertensive rats (SHR)

Show simple item record

dc.contributor.author Marangoni, Rossana Anderson
dc.contributor.author Santos, Rosangela Aparecida
dc.contributor.author Piccolo, Camila [UNIFESP]
dc.date.accessioned 2016-01-24T14:38:07Z
dc.date.available 2016-01-24T14:38:07Z
dc.date.issued 2014-11-01
dc.identifier http://dx.doi.org/10.1016/j.peptides.2014.08.016
dc.identifier.citation Peptides. New York: Elsevier B.V., v. 61, p. 69-74, 2014.
dc.identifier.issn 0196-9781
dc.identifier.uri http://repositorio.unifesp.br/handle/11600/38406
dc.description.abstract Prolylcarboxypeptidase (PRCP), an endothelial cell membrane serine peptidase that inactivates angiotensin II and activates pre-kallikrein, is thought to have anti-hypertensive and anti-proliferative roles in cardiovascular homeostasis. We hypothesized that PRCP function may be altered in heart tissue under conditions that predispose to left ventricle hypertrophy (LVH) in rats. We therefore used real-timePCR and western-blotting to examine the mRNA and protein expression of PRCP in the hearts of spontaneously hypertensive rats (SHR) at pre-hypertensive (5-week-old) and hypertensive (16-week-old) stages compared with age-matched hypertensive (2 kidney-1 clip; 2K-1C) rats and normotensive Wistar rats. PRCP mRNA expression was significantly reduced in hearts of 5- and 16-week-old SHR compared with age-matched Wistar controls, 2K-1C hypertensive rats and sham-operated normotensive rats. There were no significant differences in the PRCP mRNA and protein expression levels in hearts from hypertensive renovascular and sham-operated normotensive rats. Prolonged treatment of SHR with the AT(1) receptor antagonist losartan (40 mg/kg, gavage for 8 weeks) reduced the left ventricular weight/body weight ratio (LVW/BW), as well as the mRNA expression of collagen type 1, collagen type 3 and MMP9 in left ventricular tissue, without affecting PRCP gene and protein expression. Our results suggest that diminished PRCP gene and protein expression might be constitutionally involved in the SHR phenotype. in addition, since neither the development of arterial hypertension in the 2K-1C model nor its successful treatment in SHR altered PRCP gene and protein expression in heart tissue, it appears unlikely that PRCP function is regulated by the renin-angiotensin system or by afterload conditions. (C) 2014 Elsevier Inc. All rights reserved. en
dc.description.sponsorship Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.format.extent 69-74
dc.language.iso eng
dc.publisher Elsevier B.V.
dc.relation.ispartof Peptides
dc.rights Acesso restrito
dc.subject Heart en
dc.subject 2K-1C en
dc.subject Kallikrein-kinin system en
dc.subject Prolylcarboxypeptidase en
dc.subject Renin-angiotensin system en
dc.subject SHR en
dc.title Deficient prolylcarboxypeptidase gene and protein expression in left ventricles of spontaneously hypertensive rats (SHR) en
dc.type Artigo
dc.rights.license http://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dc.contributor.institution Universidade de São Paulo (USP)
dc.contributor.institution Universidade Federal de São Paulo (UNIFESP)
dc.description.affiliation Univ São Paulo, Dept Pharmacol, Inst Biomed Sci, BR-05508900 São Paulo, Brazil
dc.description.affiliation Universidade Federal de São Paulo, Dept Physiol, Med Sch São Paulo, UNIFESP, São Paulo, Brazil
dc.description.affiliationUnifesp Universidade Federal de São Paulo, Dept Physiol, Med Sch São Paulo, UNIFESP, São Paulo, Brazil
dc.description.sponsorshipID CNPq: CNPq 504362/2009-7
dc.identifier.doi 10.1016/j.peptides.2014.08.016
dc.description.source Web of Science
dc.identifier.wos WOS:000344232700010



File

File Size Format View

There are no files associated with this item.

This item appears in the following Collection(s)

Show simple item record

Search


Browse

Statistics

My Account