Cell adhesion molecules and eNOS expression in aorta of normocholesterolemic mice with different predispositions to atherosclerosis
Jazyk angličtina Země Japonsko Médium print-electronic
Typ dokumentu srovnávací studie, časopisecké články, práce podpořená grantem
- MeSH
- aorta enzymologie MeSH
- ateroskleróza enzymologie genetika prevence a kontrola MeSH
- druhová specificita MeSH
- fenotyp MeSH
- genetická predispozice k nemoci MeSH
- mediátory zánětu metabolismus MeSH
- molekuly buněčné adheze metabolismus MeSH
- myši inbrední C3H MeSH
- myši inbrední C57BL MeSH
- ochranné faktory MeSH
- rizikové faktory MeSH
- synthasa oxidu dusnatého, typ III metabolismus MeSH
- zvířata MeSH
- Check Tag
- ženské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- srovnávací studie MeSH
- Názvy látek
- mediátory zánětu MeSH
- molekuly buněčné adheze MeSH
- Nos3 protein, mouse MeSH Prohlížeč
- synthasa oxidu dusnatého, typ III MeSH
C57BL/6J (B6) mice were demonstrated to be the most susceptible and C3H/HeJ (C3H) mice the most resistant to development of atherosclerosis. We hypothesized, whether pro-atherogenic (P-selectin, VCAM-1, and ICAM-1) and anti-atherogenic (endoglin and eNOS) proteins are expressed differently in aorta before the onset of atherosclerosis in these two mouse strains. B6 mice (n = 16) and C3H mice (n = 16) sustained on either chow or cholesterol (1 %) diet for 8 weeks. Biochemical analysis of lipoprotein profile and Western blot analysis of P-selectin, VCAM-1, ICAM-1, eNOS, endoglin, peNOS and TGF-βRII in aorta were performed. Western blot analysis revealed a lower expression of P-selectin by 7 %, VCAM-1 by 51 %, ICAM-1 by 6 %, and a higher expression of eNOS (by 18 %) in C3H mice in comparison with B6 mice after cholesterol diet. Further analysis revealed that cholesterol diet significantly increased the expression of endoglin (by 97 %), TGF-βRII (by 50 %), eNOS (by 21 %) and peNOS (by 122 %) in C3H mice, but not in B6 mice. We propose that lower expression of P-selectin, VCAM-1 and ICAM-1 and higher expression of eNOS in vivo in aorta of C3H mice might represent another potential mechanism for C3H mice being less susceptible to atherosclerosis when compared to B6 mice. In addition, endoglin seems to be involved in an upregulation of eNOS only in C3H mice. Thus, we propose that aorta of C3H mice is less prone to the expression of pro-inflammatory and endothelial dysfunction markers when compared to B6 mice, regardless of lipoprotein profile and before any signs of atherosclerotic process.
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J Cell Biol. 1996 Jun;133(5):1109-21 PubMed
J Lipid Res. 1991 Apr;32(4):559-68 PubMed
Circ Res. 2000 May 26;86(10):1078-84 PubMed
J Clin Invest. 1993 Jun;91(6):2572-9 PubMed
Arterioscler Thromb Vasc Biol. 2000 Dec;20(12):2546-52 PubMed
Cardiovasc Res. 2006 Mar 1;69(4):845-54 PubMed
FASEB J. 2004 Mar;18(3):609-11 PubMed
Heart Vessels. 2013 May;28(3):308-15 PubMed
Arterioscler Thromb Vasc Biol. 1995 Jan;15(1):2-10 PubMed
Heart Vessels. 2012 Jul;27(4):344-51 PubMed
Proc Natl Acad Sci U S A. 1987 Jun;84(11):3763-7 PubMed
J Atheroscler Thromb. 2012;19(2):115-26 PubMed
Pharmacol Res. 2011 Jul;64(1):53-9 PubMed
Atherosclerosis. 1987 Dec;68(3):231-40 PubMed
J Nutr. 1993 Nov;123(11):1939-51 PubMed
J Cell Physiol. 2007 Sep;212(3):626-32 PubMed
Arterioscler Thromb Vasc Biol. 2007 Nov;27(11):2292-301 PubMed
Circ Res. 2005 Apr 1;96(6):684-92 PubMed
Biol Pharm Bull. 2009 Dec;32(12):1978-85 PubMed
J Clin Invest. 2001 May;107(10):1209-10 PubMed
Arteriosclerosis. 1990 Mar-Apr;10(2):316-23 PubMed
Am J Physiol Heart Circ Physiol. 2010 Oct;299(4):H959-74 PubMed
Arterioscler Thromb Vasc Biol. 1999 Aug;19(8):1960-8 PubMed
Eur Heart J. 2012 Apr;33(7):829-37, 837a-837d PubMed
Atherosclerosis. 2000 Aug;151(2):389-97 PubMed
Atherosclerosis. 2012 Sep;224(1):4-11 PubMed
Biochem Genet. 1987 Aug;25(7-8):501-11 PubMed
J Clin Invest. 2001 May;107(10):1255-62 PubMed
Atherosclerosis. 2006 Nov;189(1):99-105 PubMed
Circulation. 2000 Jul 4;102(1):75-81 PubMed
J Lipid Res. 2004 Nov;45(11):2008-14 PubMed
Circ Res. 1999 Jun 11;84(11):1237-44 PubMed
