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Role of angiotensin II in ischemia/reperfusion-induced leukocyte-endothelium interactions in the colon

Riaz, AA; Wang, Yusheng LU ; Schramm, R; Sato, T; Menger, MD; Jeppsson, Bengt LU and Thorlacius, Henrik LU (2004) In FASEB Journal 18(3). p.881-881
Abstract
The aims of the present study were to determine the effects and mechanisms of angiotensin II (Ang II) on leukocyte-endothelium interactions and the role of Ang II in a novel model of ischemia/reperfusion (I/R) in the mouse colon. Ang II dose-dependently increased leukocyte rolling and adhesion in colonic venules. Importantly, Ang II-induced leukocyte rolling was completely inhibited by immunoneutralization of P-selectin, and leukocyte adhesion was abolished in lymphocyte function antigen-1 (LFA-1)-deficient mice. The P-selectin-dependent rolling was found to be a precondition for the subsequent LFA-1-dependent leukocyte adhesion. Moreover, Ang II-induced leukocyte responses involved generation of reactive oxygen species and up-regulation... (More)
The aims of the present study were to determine the effects and mechanisms of angiotensin II (Ang II) on leukocyte-endothelium interactions and the role of Ang II in a novel model of ischemia/reperfusion (I/R) in the mouse colon. Ang II dose-dependently increased leukocyte rolling and adhesion in colonic venules. Importantly, Ang II-induced leukocyte rolling was completely inhibited by immunoneutralization of P-selectin, and leukocyte adhesion was abolished in lymphocyte function antigen-1 (LFA-1)-deficient mice. The P-selectin-dependent rolling was found to be a precondition for the subsequent LFA-1-dependent leukocyte adhesion. Moreover, Ang II-induced leukocyte responses involved generation of reactive oxygen species and up-regulation of CXC chemokines. Notably, CXC chemokines, but not Ang II, stimulated leukocyte chemotaxis in vitro. I/R increased gene expression of angiotensin converting enzyme (ACE) in the colon and plasma concentrations of Ang II. Inhibition of ACE and the type 1 angiotensin (AT(1)) receptor significantly decreased the I/R-induced leukocyte adhesion. Taken together, these novel findings demonstrate that Ang II exerts potent pro-inflammatory effects in the colonic microcirculation and that inhibition of Ang II expression or function protects against I/R-induced leukocyte responses in the colon. Thus, it is suggested that Ang II is a major target to control pathological inflammation in the colon. (Less)
Please use this url to cite or link to this publication:
author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
adhesion, inflammation, microcirculation, P-selectin
in
FASEB Journal
volume
18
issue
3
pages
881 - 881
publisher
The Federation of American Societies for Experimental Biology
external identifiers
  • wos:000220522800026
  • scopus:4644363433
ISSN
1530-6860
DOI
10.1096/fj.03-0502fje
language
English
LU publication?
yes
id
df7d981f-fd8f-46dd-9278-84dd7bd85016 (old id 283680)
date added to LUP
2007-10-26 17:04:07
date last changed
2017-05-07 04:10:57
@article{df7d981f-fd8f-46dd-9278-84dd7bd85016,
  abstract     = {The aims of the present study were to determine the effects and mechanisms of angiotensin II (Ang II) on leukocyte-endothelium interactions and the role of Ang II in a novel model of ischemia/reperfusion (I/R) in the mouse colon. Ang II dose-dependently increased leukocyte rolling and adhesion in colonic venules. Importantly, Ang II-induced leukocyte rolling was completely inhibited by immunoneutralization of P-selectin, and leukocyte adhesion was abolished in lymphocyte function antigen-1 (LFA-1)-deficient mice. The P-selectin-dependent rolling was found to be a precondition for the subsequent LFA-1-dependent leukocyte adhesion. Moreover, Ang II-induced leukocyte responses involved generation of reactive oxygen species and up-regulation of CXC chemokines. Notably, CXC chemokines, but not Ang II, stimulated leukocyte chemotaxis in vitro. I/R increased gene expression of angiotensin converting enzyme (ACE) in the colon and plasma concentrations of Ang II. Inhibition of ACE and the type 1 angiotensin (AT(1)) receptor significantly decreased the I/R-induced leukocyte adhesion. Taken together, these novel findings demonstrate that Ang II exerts potent pro-inflammatory effects in the colonic microcirculation and that inhibition of Ang II expression or function protects against I/R-induced leukocyte responses in the colon. Thus, it is suggested that Ang II is a major target to control pathological inflammation in the colon.},
  author       = {Riaz, AA and Wang, Yusheng and Schramm, R and Sato, T and Menger, MD and Jeppsson, Bengt and Thorlacius, Henrik},
  issn         = {1530-6860},
  keyword      = {adhesion,inflammation,microcirculation,P-selectin},
  language     = {eng},
  number       = {3},
  pages        = {881--881},
  publisher    = {The Federation of American Societies for Experimental Biology},
  series       = {FASEB Journal},
  title        = {Role of angiotensin II in ischemia/reperfusion-induced leukocyte-endothelium interactions in the colon},
  url          = {http://dx.doi.org/10.1096/fj.03-0502fje},
  volume       = {18},
  year         = {2004},
}