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

11 Scopus citations

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

Keywords

  • Atherosclerosis
  • ERK1/2
  • Inflammation
  • MAPK
  • MCMV
  • p38

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Genetics
  • Genetics(clinical)
  • Molecular Medicine
  • Pharmaceutical Science

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