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J Neurochem. 2011 Jul;118(1):93-104. doi: 10.1111/j.1471-4159.2011.07203.x. Epub 2011 Mar 14.

CCAAT/enhancer binding protein β expression is increased in the brain during HIV-1-infection and contributes to regulation of astrocyte tissue inhibitor of metalloproteinase-1.

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  • 1Department of Cell Biology and Anatomy, University of North Texas Health Science Center, Fort Worth, TX, USA.


Human immunodeficiency virus (HIV)-1-associated neurocognitive disorders (HAND) associated with infection and activation of mononuclear phagocytes (MP) in the brain, occur late in disease. Infected/activated MP initiate neuroinflammation activating glial cells and ultimately disrupting neuronal function. Astrocytes secrete tissue inhibitor of metalloproteinase (TIMP)-1 in response to neural injury. Altered TIMP-1 levels are implicated in several CNS diseases. CCAAT enhancer-binding protein β (C/EBPβ), a transcription factor, is expressed in rodent brains in response to neuroinflammation, implicating it in Alzheimer's, Parkinson's, and HAND. Here, we report that C/EBPβ mRNA levels are elevated and its isoforms differentially expressed in total brain tissue lysates of HIV-1-infected and HIV-1 encephalitis patients. In vitro, HAND-relevant stimuli additively induce C/EBPβ nuclear expression in human astrocytes through 7 days of treatment. Over-expression of C/EBPβ increases TIMP-1 promoter activity, mRNA, and protein levels in human astrocytes activated with interleukin-1β. Knockdown of C/EBPβ with siRNA decreases TIMP-1 mRNA and protein levels. These data suggest that C/EBPβ isoforms are involved in complex regulation of astrocyte TIMP-1 production during HIV-1 infection; however, further studies are required to completely understand their role during disease progression.

© 2011 The Authors. Journal of Neurochemistry © 2011 International Society for Neurochemistry.

[PubMed - indexed for MEDLINE]
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