Murine cytomegalovirus (MCMV) infection upregulates P38 MAP kinase in aortas of Apo e KO Mice: A molecular mechanism for mcmv-induced acceleration of atherosclerosis

Yajarayma J. Tang-Feldman, Stephanie R. Lochhead, G. Raymond Lochhead, Cindy Yu, Michael George, Amparo C Villablanca, Claire Pomeroy

Research output: Contribution to journalArticle

10 Citations (Scopus)

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 languageEnglish (US)
Pages (from-to)54-64
Number of pages11
JournalJournal of Cardiovascular Translational Research
Volume6
Issue number1
DOIs
StatePublished - Feb 2013

Fingerprint

Muromegalovirus
Cytomegalovirus Infections
p38 Mitogen-Activated Protein Kinases
Knockout Mice
Aorta
Atherosclerosis
Up-Regulation
Vascular Cell Adhesion Molecule-1
Apolipoproteins E
Virus Diseases
Intercellular Adhesion Molecule-1
Viral Load
Genes
Viruses
Gene Expression

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 journalArticle

Tang-Feldman, Yajarayma J. ; Lochhead, Stephanie R. ; Lochhead, G. Raymond ; Yu, Cindy ; George, Michael ; Villablanca, Amparo C ; Pomeroy, Claire. / Murine cytomegalovirus (MCMV) infection upregulates P38 MAP kinase in aortas of Apo e KO Mice : A molecular mechanism for mcmv-induced acceleration of atherosclerosis. In: Journal of Cardiovascular Translational Research. 2013 ; Vol. 6, No. 1. pp. 54-64.
@article{a3cb839cf3294d0a899f15916e4974d4,
title = "Murine cytomegalovirus (MCMV) infection upregulates P38 MAP kinase in aortas of Apo e KO Mice: A molecular mechanism for mcmv-induced acceleration of atherosclerosis",
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.",
keywords = "Atherosclerosis, ERK1/2, Inflammation, MAPK, MCMV, p38",
author = "Tang-Feldman, {Yajarayma J.} and Lochhead, {Stephanie R.} and Lochhead, {G. Raymond} and Cindy Yu and Michael George and Villablanca, {Amparo C} and Claire Pomeroy",
year = "2013",
month = "2",
doi = "10.1007/s12265-012-9428-x",
language = "English (US)",
volume = "6",
pages = "54--64",
journal = "Journal of Cardiovascular Translational Research",
issn = "1937-5387",
publisher = "Springer New York",
number = "1",

}

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 -