Upregulation of junctional adhesion molecule-A is a putative prognostic marker of hypertension

Upregulation of junctional adhesion molecule-A is a putative prognostic marker of hypertension

Author Xu, Haibo Google Scholar
Oliveira-Sales, Elizabeth Barbosa de Autor UNIFESP Google Scholar
McBride, Fiona Google Scholar
Liu, Beihui Google Scholar
Hewinson, James Google Scholar
Toward, Marie Google Scholar
Hendy, Emma B. Google Scholar
Graham, Delyth Google Scholar
Dominiczak, Anna F. Google Scholar
Giannotta, Monica Google Scholar
Waki, Hidefumi Google Scholar
Ascione, Raimondo Google Scholar
Paton, Julian Francis Richmond Google Scholar
Kasparov, Sergey Google Scholar
Institution Univ Bristol
Universidade Federal de São Paulo (UNIFESP)
Univ Glasgow
Inst FIRC Mol Oncol
Wakayama Med Univ
Abstract Establishing biochemical markers of pre-hypertension and early hypertension could help earlier diagnostics and therapeutic intervention. We assess dynamics of junctional adhesion molecule-A (JAM-A) expression in rat models of hypertension and test whether JAM-A expression could be driven by angiotensin (ANG) II and whether JAM-A contributes to the progression of hypertension. We also compare JAM-A expression in normo- and hypertensive humans.In pre-hypertensive and spontaneously hypertensive rats (SHRs), JAM-A protein was overexpressed in the brainstem microvasculature, lung, liver, kidney, spleen, and heart. JAM-A upregulation at early and late stages was even greater in the stroke-prone SHR. However, JAM-A was not upregulated in leucocytes and platelets of SHRs. in Goldblatt 2K-1C hypertensive rats, JAM-A expression was augmented before any increase in blood pressure, and similarly JAM-A upregulation preceded hypertension caused by peripheral and central ANG II infusions. in SHRs, ANG II type 1 (AT(1)) receptor antagonism reduced JAM-A expression, but the vasodilator hydralazine did not. Body-wide downregulation of JAM-A with Vivo-morpholinos in juvenile SHRs delayed the progression of hypertension. in the human saphenous vein, JAM-A mRNA was elevated in hypertensive patients with untreated hypertension compared with normotensive patients but reduced in patients treated with reninangiotensin system antagonists.Body-wide upregulation of JAM-A in genetic and induced models of hypertension in the rat precedes the stable elevation of arterial pressure. JAM-A upregulation may be triggered by AT(1) receptor-mediated signalling. An association of JAM-A with hypertension and sensitivity to blockers of ANG II signalling were also evident in humans. We suggest a prognostic and possibly a pathogenic role of JAM-A in arterial hypertension.
Keywords Adhesion molecules
JAM-A
Hypertension
Angiotensin
Vasculature
Language English
Sponsor British Heart Foundation
Grant number British Heart Foundation: PG/06/085
British Heart Foundation: RG/07/006
Date 2012-12-01
Published in Cardiovascular Research. Oxford: Oxford Univ Press, v. 96, n. 3, p. 552-560, 2012.
ISSN 0008-6363 (Sherpa/Romeo, impact factor)
Publisher Oxford Univ Press
Extent 552-560
Origin http://dx.doi.org/10.1093/cvr/cvs273
Access rights Open access Open Access
Type Article
Web of Science ID WOS:000311306800026
URI http://repositorio.unifesp.br/handle/11600/35524

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