miR-181a and inflammation: miRNA homeostasis response to inflammatory stimuli in vivo

Biochem Biophys Res Commun. 2013 Jan 11;430(2):647-52. doi: 10.1016/j.bbrc.2012.11.097. Epub 2012 Dec 5.


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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Diabetes Mellitus, Experimental / immunology
  • Diabetes Mellitus, Type 1 / immunology
  • Disease Models, Animal
  • Gene Knockdown Techniques
  • Homeostasis*
  • Humans
  • Inflammation / immunology*
  • Interleukin-1alpha / metabolism
  • Interleukin-1beta / metabolism
  • Interleukin-6 / metabolism
  • Lipopolysaccharides / immunology
  • Macrophages, Peritoneal / immunology
  • Male
  • Mice
  • Mice, Inbred BALB C
  • MicroRNAs / metabolism*
  • Toll-Like Receptor 4 / genetics
  • Toll-Like Receptor 4 / metabolism
  • Tumor Necrosis Factor-alpha / metabolism


  • Interleukin-1alpha
  • Interleukin-1beta
  • Interleukin-6
  • Lipopolysaccharides
  • MicroRNAs
  • Tlr4 protein, mouse
  • Toll-Like Receptor 4
  • Tumor Necrosis Factor-alpha
  • mirn181 microRNA, mouse