title: MicroRNA-155 Promotes Atherosclerosis  Inflammation via Targeting SOCS1.
abstract: OBJECTIVE
  Accumulating evidence suggests that atherosclerotic progression depends on persistent and chronic inflammation in the arterial walls. MicroRNA-155 is reportedly involved in cardiovascular disease and has been implicated as a pro-inflammation regulator. Although some researchers have focused on microRNA-155 as an atherosclerosis regulator, the mechanisms by which microRNA-155 functions as a putative pro-atherosclerosis microRNA are largely unknown. This study aims to analyze microRNA-155's effects on atherosclerotic inflammation and to explore its mechanism.
  
  
  METHODS
  MicroRNA-155's effects on atherosclerotic inflammation were observed along with the expression and activity levels of SOCS1, STAT3 and NF-κB though microRNA-155 inhibition or overexpression.
  
  
  RESULTS
  Highly expressions of microRNA-155 in oxLDL-stimulated macrophages and atherosclerosis mice were inversely correlated with SOCS1 expression. Ectopic microRNA-155 overexpression significantly promoted inflammatory cytokine and chemokine production and atherosclerosis progression. We then observed microRNA-155's functional role in the atherosclerotic pathophysiological process in vivo and in vitro. The observation revealed that by enhancing STAT3 and NF-κB signaling and facilitating immune inflammation by targeting SOCS1, microRNA-155 plays a promotable role in atherosclerosis progression.
  
  
  CONCLUSIONS
  microRNA-155 works as a promoter in the atherosclerotic procession. Its mechanism may include enhancing inflammatory response in atherosclerosis by increasing STAT3 and NF-κB signaling via targeting SOCS1.
authors.forename: Yang
authors.initials: Y
authors.lastname: Yang
authors.forename: Lixia
authors.initials: L
authors.lastname: Yang
authors.forename: Xing
authors.initials: X
authors.lastname: Liang
authors.forename: Guofu
authors.initials: G
authors.lastname: Zhu
mesh_terms: D000818:Animals; D050197:Atherosclerosis / Q000150:complications* / Q000235:genetics* / Q000276:immunology / Q000473:pathology; D001483:Base Sequence; D002460:Cell Line; D002465:Cell Movement; D005786:Gene Expression Regulation; D006801:Humans; D007249:Inflammation / Q000150:complications* / Q000235:genetics* / Q000276:immunology / Q000473:pathology; D008077:Lipoproteins, LDL / Q000276:immunology; D008264:Macrophages / Q000276:immunology / Q000378:metabolism; D008297:Male; D008810:Mice, Inbred C57BL; D035683:MicroRNAs / Q000235:genetics* / Q000276:immunology; D016328:NF-kappa B / Q000276:immunology; D050796:STAT3 Transcription Factor / Q000276:immunology; D015398:Signal Transduction; D000071222:Suppressor of Cytokine Signaling 1 Protein; D050826:Suppressor of Cytokine Signaling Proteins / Q000235:genetics* / Q000276:immunology
chemical_list: D008077:Lipoproteins, LDL; C524942:MIRN155 microRNA, human; D035683:MicroRNAs; D016328:NF-kappa B; C108944:SOCS1 protein, human; D050796:STAT3 Transcription Factor; D000071222:Suppressor of Cytokine Signaling 1 Protein; D050826:Suppressor of Cytokine Signaling Proteins; C099252:oxidized low density lipoprotein