title: miR-181a and inflammation: miRNA homeostasis response to inflammatory stimuli in vivo.
abstract: Inflammatory stimuli are usually associated with homeostatic responses, which have an important function in protecting the body from excessive inflammatory damage. Previous studies reported the anti-inflammatory effect of miR-181a. The current study utilized two animal models of inflammation, induced by either lipopolysaccharides (LPS) or streptozotocin. We demonstrated that inflammatory stimuli significantly increase miR-181a expression, concurrently with inflammatory factors. In addition, the knock down of toll-like receptor 4 (TLR-4) by small interfering RNA in LPS-induced Raw264.7 cells significantly reduces the expression of both miR-181a and inflammatory factors. Furthermore, patients with inflammatory response show increased expression of miR-181a, which is strongly correlated with the expression of interleukin (IL)-1β, IL-6, and tumor necrosis factor alpha. These data indicate that the up-regulation of miR-181a may be associated with homeostatic response to inflammatory stimuli by TLR-4 pathway activation. Therefore, miR-181a may serve as a novel marker for inflammatory response.
authors.affiliation: Shenzhen Key Lab of Health Science and Technology, Division of Life Science & Health, Graduate School at Shenzhen, Tsinghua University, Shenzhen 518055, China.
authors.forename: Weidong
authors.initials: W
authors.lastname: Xie
authors.forename: Zhongxin
authors.initials: Z
authors.lastname: Li
authors.forename: Mengnan
authors.initials: M
authors.lastname: Li
authors.forename: Naihan
authors.initials: N
authors.lastname: Xu
authors.forename: Yaou
authors.initials: Y
authors.lastname: Zhang
mesh_terms: D000818:Animals; D003921:Diabetes Mellitus, Experimental / Q000276:immunology; D003922:Diabetes Mellitus, Type 1 / Q000276:immunology; D004195:Disease Models, Animal; D055785:Gene Knockdown Techniques; D006706:Homeostasis; D006801:Humans; D007249:Inflammation / Q000276:immunology*; D053582:Interleukin-1alpha / Q000378:metabolism; D053583:Interleukin-1beta / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D008070:Lipopolysaccharides / Q000276:immunology; D017737:Macrophages, Peritoneal / Q000276:immunology; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D035683:MicroRNAs / Q000378:metabolism*; D051197:Toll-Like Receptor 4 / Q000235:genetics / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D053582:Interleukin-1alpha; D053583:Interleukin-1beta; D015850:Interleukin-6; D008070:Lipopolysaccharides; D035683:MicroRNAs; C493487:Tlr4 protein, mouse; D051197:Toll-Like Receptor 4; D014409:Tumor Necrosis Factor-alpha; C529100:mirn181 microRNA, mouse