dc.contributor.author |
Xu, H |
en |
dc.contributor.author |
Oliveira-Sales, EB |
en |
dc.contributor.author |
McBryde, Fiona |
en |
dc.contributor.author |
Liu, B |
en |
dc.contributor.author |
Hewinson, J |
en |
dc.contributor.author |
Toward, M |
en |
dc.contributor.author |
Hendy, EB |
en |
dc.contributor.author |
Graham, D |
en |
dc.contributor.author |
Dominiczak, AF |
en |
dc.contributor.author |
Giannotta, M |
en |
dc.contributor.author |
Waki, H |
en |
dc.contributor.author |
Ascione, R |
en |
dc.contributor.author |
Paton, Julian |
en |
dc.contributor.author |
Kasparov, S |
en |
dc.date.accessioned |
2014-01-13T01:57:14Z |
en |
dc.date.issued |
2012-12-01 |
en |
dc.identifier.citation |
Cardiovascular Research 96(3):552-560 01 Dec 2012 |
en |
dc.identifier.issn |
0008-6363 |
en |
dc.identifier.uri |
http://hdl.handle.net/2292/21385 |
en |
dc.description.abstract |
Aims 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. Methods and results 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 (AT1) 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 renin–angiotensin system antagonists. Conclusion 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 AT1 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. |
en |
dc.language |
aa |
en |
dc.relation.ispartofseries |
Cardiovascular Research |
en |
dc.rights |
Items in ResearchSpace are protected by copyright, with all rights reserved, unless otherwise indicated. Previously published items are made available in accordance with the copyright policy of the publisher. Details obtained from http://www.oxfordjournals.org/access_purchase/publication_rights.html http://www.sherpa.ac.uk/romeo/issn/0008-6363/ |
en |
dc.rights.uri |
https://researchspace.auckland.ac.nz/docs/uoa-docs/rights.htm |
en |
dc.title |
Upregulation of junctional adhesion molecule-A is a putative prognostic marker of hypertension |
en |
dc.type |
Journal Article |
en |
dc.identifier.doi |
10.1093/cvr/cvs273 |
en |
pubs.issue |
3 |
en |
pubs.begin-page |
552 |
en |
pubs.volume |
96 |
en |
dc.identifier.pmid |
22918977 |
en |
pubs.end-page |
560 |
en |
dc.rights.accessrights |
http://purl.org/eprint/accessRights/RestrictedAccess |
en |
pubs.subtype |
Article |
en |
pubs.elements-id |
413824 |
en |
pubs.org-id |
Medical and Health Sciences |
en |
pubs.org-id |
Medical Sciences |
en |
pubs.org-id |
Physiology Division |
en |
pubs.record-created-at-source-date |
2014-01-13 |
en |
pubs.dimensions-id |
22918977 |
en |