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

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 tissu...

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Published in:Peptides (New York, N.Y. : 1980) N.Y. : 1980), 2014-11, Vol.61, p.69-74
Main Authors: Marangoni, Rossana Anderson, Santos, Rosangela Aparecida, Piccolo, Camila
Format: Article
Language:English
Subjects:
2K-1C
Animals
Carboxypeptidases - biosynthesis
Collagens
Gene expression
Gene Expression Regulation, Enzymologic
Genes
Heart
Heart Ventricles - enzymology
Heart Ventricles - pathology
Hypertension - enzymology
Hypertension - pathology
Kallikrein–kinin system
Mathematical models
Myocardium - enzymology
Myocardium - pathology
Peptides
Prolylcarboxypeptidase
Proteins
Rats
Rats, Inbred SHR
Renin-Angiotensin System
RNA, Messenger - biosynthesis
SHR
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Summary: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-time PCR 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 AT1 receptor antagonist losartan (40mg/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.
ISSN:0196-9781
1873-5169
DOI:10.1016/j.peptides.2014.08.016