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Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 J+Immunol 2016 ; 196 (6): 2799-808 Nephropedia Template TP
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LincRNA-Cox2 Promotes Late Inflammatory Gene Transcription in Macrophages through Modulating SWI/SNF-mediated Chromatin Remodeling #MMPMID26880762
Hu G; Gong AY; Wang Y; Ma S; Chen X; Chen J; Su CJ; Shibata A; Strauss-Soukup JK; Drescher KM; Chen XM
J Immunol 2016[Mar]; 196 (6): 2799-808 PMID26880762show ga
LincRNAs are long non-coding transcripts (>200 nt) from the intergenic regions of annotated protein-coding genes. One of the most highly induced lincRNAs in macrophages upon TLR ligation is lincRNA-Cox2, which has recently been shown to mediate both the activation and repression of distinct classes of immune genes in innate immune cells. We report here that lincRNA-Cox2 located at chromosome 1 proximal to the prostaglandin-endoperoxide synthase 2 (Ptgs2/Cox2) gene is an early-primary inflammatory gene controlled by NF-?B signaling in murine macrophages. Functionally, lincRNA-Cox2 is required for the transcription of NF-?B-regulated late-primary inflammatory response genes stimulated by bacterial lipopolysaccharide. Specifically, lincRNA-Cox2 is assembled into the SWI/SNF (SWItch/Sucrose NonFermentable) complex in cells after lipopolysaccharide stimulation. This resulting lincRNA-Cox2/SWI/SNF complex can modulate the assembly of NF-?B subunits to the SWI/SNF complex, and ultimately, SWI/SNF-associated chromatin remodeling and transactivation of the late-primary inflammatory response genes in macrophages in response to microbial challenge. Therefore, our data indicate a new regulatory role of NF-?B-induced lincRNA-Cox2 to act as a co-activator of NF-?B for the transcription of late-primary response genes in innate immune cells through modulation of epigenetic chromatin remodeling.