TAILIEUCHUNG - Báo cáo khoa học: Fragile X-related protein FXR1 controls posttranscriptional suppression of lipopolysaccharide-induced tumour necrosis factor-a production by transforming growth factor-b1

Tumour necrosis factor-a(TNF-a) is a key mediator of inflammation in host defence against infection and in autoimmune disease. Its production is controlled post-transcriptionally by multiple RNA-binding proteins that interact with the TNF-aAU-rich element and regulate its expression; one of these is Fragile X mental retardation-related protein 1 (FXR1). | Fragile X-related protein FXR1 controls post-transcriptional suppression of lipopolysaccharide-induced tumour necrosis factor-a production by transforming growth factor-p1 Tarnjit K. Khera1 Andrew D. Dick1 2 and Lindsay B. Nicholson1 2 1 Department of Cellular and Molecular Medicine Schoolof MedicalSciences University of Bristol UK 2 Department of ClinicalSciences South Bristol Academic Unit of Ophthalmology University of Bristol UK Keywords FXR1 macrophages RNA-binding proteins TGF-P1 TNF-a Correspondence T. K. Khera Department of Cellular and Molecular Medicine Schoolof Medical Sciences University Walk Bristol BS8 1TD UK Fax 44 117 3312091 Tel 44 117 3312012 E-mail Website http cellmolmed air Received 26 February 2010 revised 11 April 2010 accepted 20 April 2010 doi Tumour necrosis factor-a TNF-a is a key mediator of inflammation in host defence against infection and in autoimmune disease. Its production is controlled post-transcriptionally by multiple RNA-binding proteins that interact with the TNF-a AU-rich element and regulate its expression one of these is Fragile X mental retardation-related protein 1 FXR1 . The anti-inflammatory cytokine transforming growth factor-b1 TGF-b1 which is involved in the homeostatic regulation of TNF-a causes post-transcriptional suppression of lipopolysaccharide LPS -induced TNF-a production. We report here that this depends on FXR1. Using RAW cells and bone marrow-derived macrophages BMDMu stimulated with LPS and TGF-b1 we show that TGF-b1 inhibits TNF-a protein secretion whereas TNF-a mRNA expression remains unchanged. This response is recapitulated by the 3 -UTR of TNF-a which is known to bind FXR1. TGF-b1 induces FXR1 with a pattern of expression distinct from that of tristetraprolin T-cell intracellular antigen 1 or human antigen R. When FXR1 is knocked down TGF-b1 is no longer able to inhibit LPS-induced TNF-a protein production and overexpression

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