Abstract
Multiple studies suggest an association between cytomegalovirus (CMV) infection and atherogenesis; however, the molecular mechanisms by which viral infection might exacerbate atherosclerosis are not well understood. Aortas of MCMV-infected and uninfected Apo E knockout (KO) mice were analyzed for atherosclerotic lesion development and differential gene expression. Lesions in the infected mice were larger and showed more advanced disease compared to the uninfected mice. Sixty percent of the genes in the MAPK pathway were upregulated in the infected mice. p38 and ERK 1/2 MAPK genes were 5.6- and 2.0-fold higher, respectively, in aortas of infected vs. uninfected mice. Levels of VCAM-1, ICAM-1, and MCP-1 were ~2.0-2.6-fold higher in aortas of infected vs. uninfected mice. Inhibition of p38 with SB203580 resulted in lower levels of pro-atherogenic molecules and MCMV viral load in aortas of infected mice. MCMV-induced upregulation of p38 may drive the virus-induced acceleration of atherogenesis observed in our model.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 54-64 |
| Number of pages | 11 |
| Journal | Journal of Cardiovascular Translational Research |
| Volume | 6 |
| Issue number | 1 |
| DOIs | |
| State | Published - Feb 2013 |
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Keywords
- Atherosclerosis
- ERK1/2
- Inflammation
- MAPK
- MCMV
- p38
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
- Genetics
- Genetics(clinical)
- Molecular Medicine
- Pharmaceutical Science
Cite this
Murine cytomegalovirus (MCMV) infection upregulates P38 MAP kinase in aortas of Apo e KO Mice : A molecular mechanism for mcmv-induced acceleration of atherosclerosis. / Tang-Feldman, Yajarayma J.; Lochhead, Stephanie R.; Lochhead, G. Raymond; Yu, Cindy; George, Michael; Villablanca, Amparo C; Pomeroy, Claire.
In: Journal of Cardiovascular Translational Research, Vol. 6, No. 1, 02.2013, p. 54-64.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Murine cytomegalovirus (MCMV) infection upregulates P38 MAP kinase in aortas of Apo e KO Mice
T2 - A molecular mechanism for mcmv-induced acceleration of atherosclerosis
AU - Tang-Feldman, Yajarayma J.
AU - Lochhead, Stephanie R.
AU - Lochhead, G. Raymond
AU - Yu, Cindy
AU - George, Michael
AU - Villablanca, Amparo C
AU - Pomeroy, Claire
PY - 2013/2
Y1 - 2013/2
N2 - Multiple studies suggest an association between cytomegalovirus (CMV) infection and atherogenesis; however, the molecular mechanisms by which viral infection might exacerbate atherosclerosis are not well understood. Aortas of MCMV-infected and uninfected Apo E knockout (KO) mice were analyzed for atherosclerotic lesion development and differential gene expression. Lesions in the infected mice were larger and showed more advanced disease compared to the uninfected mice. Sixty percent of the genes in the MAPK pathway were upregulated in the infected mice. p38 and ERK 1/2 MAPK genes were 5.6- and 2.0-fold higher, respectively, in aortas of infected vs. uninfected mice. Levels of VCAM-1, ICAM-1, and MCP-1 were ~2.0-2.6-fold higher in aortas of infected vs. uninfected mice. Inhibition of p38 with SB203580 resulted in lower levels of pro-atherogenic molecules and MCMV viral load in aortas of infected mice. MCMV-induced upregulation of p38 may drive the virus-induced acceleration of atherogenesis observed in our model.
AB - Multiple studies suggest an association between cytomegalovirus (CMV) infection and atherogenesis; however, the molecular mechanisms by which viral infection might exacerbate atherosclerosis are not well understood. Aortas of MCMV-infected and uninfected Apo E knockout (KO) mice were analyzed for atherosclerotic lesion development and differential gene expression. Lesions in the infected mice were larger and showed more advanced disease compared to the uninfected mice. Sixty percent of the genes in the MAPK pathway were upregulated in the infected mice. p38 and ERK 1/2 MAPK genes were 5.6- and 2.0-fold higher, respectively, in aortas of infected vs. uninfected mice. Levels of VCAM-1, ICAM-1, and MCP-1 were ~2.0-2.6-fold higher in aortas of infected vs. uninfected mice. Inhibition of p38 with SB203580 resulted in lower levels of pro-atherogenic molecules and MCMV viral load in aortas of infected mice. MCMV-induced upregulation of p38 may drive the virus-induced acceleration of atherogenesis observed in our model.
KW - Atherosclerosis
KW - ERK1/2
KW - Inflammation
KW - MAPK
KW - MCMV
KW - p38
UR - http://www.scopus.com/inward/record.url?scp=84872604356&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84872604356&partnerID=8YFLogxK
U2 - 10.1007/s12265-012-9428-x
DO - 10.1007/s12265-012-9428-x
M3 - Article
C2 - 23192592
AN - SCOPUS:84872604356
VL - 6
SP - 54
EP - 64
JO - Journal of Cardiovascular Translational Research
JF - Journal of Cardiovascular Translational Research
SN - 1937-5387
IS - 1
ER -