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A 3 adenosine receptor deficiency does not influence atherogenesis
Author(s) -
Jones Matthew R.,
Zhao Zhihui,
Sullivan Christopher P.,
Schreiber Barbara M.,
Stone Phillip J.,
Toselli Paul A.,
Kagan Herbert M.,
Cohen Richard A.,
Ravid Katya
Publication year - 2004
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.20122
Subject(s) - inflammation , medicine , endocrinology , vascular smooth muscle , receptor , mast cell , lesion , in vivo , biology , chemistry , immunology , pathology , smooth muscle , microbiology and biotechnology
Atherosclerosis is a multifactorial disease, the progression of which is modulated by several factors, including inflammation and hypercholesterolemia. The A 3 adenosine receptor (A 3 AR) has been reported to affect mast cell degranulation leading to inflammation, as well as to influence cardiovascular homeostasis. Here, we show that its deletion can also impact vascular smooth muscle cell (VSMC) proliferation in vitro. Based on these observations, we hypothesized that A 3 AR deficiency would affect atheromatous lesion development in vivo. Our results indicate that the expression of the matrix enzyme lysyl oxidase (LO) is increased while the proliferation potential of VSMC is decreased in A 3 AR‐null aortas. This is in accordance with the previously reported inverse correlation between LO level and proliferation. Nevertheless, we found that A 3 ‐deficiency does not protect vessels against atherogenesis. This was demonstrated in mouse models of high fat diet‐induced atherosclerosis and guidewire‐induced femoral artery injury. We conclude that the contributions of the A 3 AR to inflammation and to modulating LO levels are not significant enough to control vascular response to injury. © 2004 Wiley‐Liss, Inc.