TGF-beta1 reduces the heterogeneity of astrocytic cyclooxygenase-2 and nitric oxide synthase-2 gene expression in a stimulus-independent manner

Prostaglandins & Other Lipid Mediators
Mary E HambySandra J Hewett

Abstract

Transforming growth factor-beta1 (TGF-beta1) is upregulated by inflammatory mediators in several neurological diseases/disorders where it either participates in the pathology or provides protection. Often, the biological outcome of TGF-beta1 is dependent upon changes in gene expression. Recently, we demonstrated that TGF-beta1 enhances astrocytic nitric oxide production induced by lipopolysaccharide (LPS) plus interferon-gamma (IFNgamma) by increasing the number of astrocytes in a population that express NOS-2. The purpose of this study was twofold: (1) to determine whether this effect occurs more generally by assessing the effect of TGF-beta1 on another pro-inflammatory gene, cyclooxygenase-2 (COX-2); and (2) to assess stimulus specificity. We found that TGF-beta1 augmented LPS plus IFNgamma-induced COX-2 mRNA and protein expression, by nearly tripling the number of astrocytes that express COX-2. The effect was not stimulus-specific as TGF-beta1 enhanced the number of astrocytes that expressed both COX-2 and NOS-2 protein when either IL-1beta or TNFalpha was used in lieu of LPS. Collectively, these results suggest that TGF-beta1 augments overall protein expression levels of select pro-inflammatory genes in astrocytes in a prom...Continue Reading

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Citations

Oct 1, 2010·Neurotherapeutics : the Journal of the American Society for Experimental NeuroTherapeutics·Mary E Hamby, Michael V Sofroniew
Oct 19, 2012·The Journal of Neuroscience : the Official Journal of the Society for Neuroscience·Mary E HambyMichael V Sofroniew
Sep 10, 2014·European Journal of Orthopaedic Surgery & Traumatology : Orthopédie Traumatologie·Kun ZhangPeizhen Lv
May 25, 2011·Free Radical Biology & Medicine·Christie J BrunoHarry Ischiropoulos

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