Src family kinases participate in the regulation of encephalomyocarditis virus-induced cyclooxygenase-2 expression by macrophages. J Gen Virol 2010 Sep;91(Pt 9):2278-85
Date
05/28/2010Pubmed ID
20505008Pubmed Central ID
PMC3052521DOI
10.1099/vir.0.022665-0Scopus ID
2-s2.0-77956272628 (requires institutional sign-in at Scopus site) 11 CitationsAbstract
Src family kinases (SFKs) are non-receptor tyrosine kinases that have been implicated as regulators of the inflammatory response. In this study, the role of SFK activation in the inflammatory response of macrophages to encephalomyocarditis virus (EMCV) infection was examined. Virus infection of macrophages stimulates the expression of cyclooxygenase-2 (COX-2), interleukin (IL)-1beta and inducible nitric oxide synthase (iNOS). Inhibition of SFK attenuates EMCV-induced COX-2 expression and prostaglandin E(2) production, iNOS expression and subsequent nitric oxide production, and IL-1beta expression. EMCV-induced COX-2 expression requires the activation of nuclear factor-kappaB and the mitogen-activated protein kinase p38. Consistent with these previous findings, inhibition of SFKs attenuated the phosphorylation of p38 in response to EMCV infection, suggesting that SFKs may act upstream of p38. These findings provide evidence that SFK activation plays an active role in the regulation of inflammatory gene expression by virus-infected macrophages.
Author List
Freudenburg W, Buller RM, Corbett JAAuthor
John A. Corbett PhD Professor in the Biochemistry department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AnimalsBase Sequence
Cell Line
Cyclooxygenase 2
DNA Primers
Dinoprostone
Encephalomyocarditis virus
Enzyme Activation
Host-Pathogen Interactions
I-kappa B Proteins
Inflammation Mediators
Interleukin-1beta
Macrophages
Mice
Models, Biological
NF-KappaB Inhibitor alpha
NF-kappa B
Nitric Oxide
Nitric Oxide Synthase Type II
RNA, Messenger
Transcriptional Activation
p38 Mitogen-Activated Protein Kinases
src-Family Kinases
