title: miR-155 Regulated Inflammation Response by the SOCS1-STAT3-PDCD4 Axis in Atherogenesis.
abstract: Inflammation response plays a critical role in all phases of atherosclerosis (AS). Increased evidence has demonstrated that miR-155 mediates inflammatory mediators in macrophages to promote plaque formation and rupture. However, the precise mechanism of miR-155 remains unclear in AS. Here, we also found that miR-155 and PDCD4 were elevated in the aortic tissue of atherosclerotic mice and ox-LDL treated RAW264.7 cells. Further studies showed that miR-155 not only directly inhibited SOCS1 expression, but also increased the expression of p-STAT and PDCD4, as well as the production of proinflammation mediators IL-6 and TNF-α. Downregulation of miR-155 and PDCD4 and upregulation of SOCS1 obviously decreased the IL-6 and TNF-αexpression. In addition, inhibition of miR-155 levels in atherosclerotic mice could notably reduce the IL-6 and TNF-αlevel in plasma and aortic tissue, accompanied with increased p-STAT3 and PDCD4 and decreased SOCS1. Thus, miR-155 might mediate the inflammation in AS via the SOCS1-STAT3-PDCD4 axis. These results provide a rationale for intervention of intracellular miR-155 as possible antiatherosclerotic targets.
authors.affiliation: Department of Postgraduate, Third Military Medical University, Chongqing 400038, China; Department of Cardiology, Kunming General Hospital of Chengdu Military Area, Yunnan 650032, China.
authors.forename: Jinshan
authors.initials: J
authors.lastname: Ye
authors.affiliation: Department of Cardiology, Kunming General Hospital of Chengdu Military Area, Yunnan 650032, China.
authors.forename: Ruiwei
authors.initials: R
authors.lastname: Guo
authors.affiliation: Department of Cardiology, Kunming General Hospital of Chengdu Military Area, Yunnan 650032, China.
authors.forename: Yankun
authors.initials: Y
authors.lastname: Shi
authors.affiliation: Department of Cardiology, Kunming General Hospital of Chengdu Military Area, Yunnan 650032, China.
authors.forename: Feng
authors.initials: F
authors.lastname: Qi
authors.affiliation: Department of Cardiology, Kunming General Hospital of Chengdu Military Area, Yunnan 650032, China.
authors.forename: Chuanming
authors.initials: C
authors.lastname: Guo
authors.affiliation: Department of Postgraduate, Third Military Medical University, Chongqing 400038, China; Department of Cardiology, Kunming General Hospital of Chengdu Military Area, Yunnan 650032, China.
authors.forename: Lixia
authors.identifier: 0000-0001-6000-5784
authors.initials: L
authors.lastname: Yang
mesh_terms: D000818:Animals; D001011:Aorta / Q000378:metabolism; D001057:Apolipoproteins E / Q000378:metabolism; D051017:Apoptosis Regulatory Proteins / Q000378:metabolism*; D050197:Atherosclerosis / Q000378:metabolism*; D007249:Inflammation / Q000378:metabolism*; D008297:Male; D051379:Mice; D035683:MicroRNAs / Q000378:metabolism*; D000067996:RAW 264.7 Cells; D034741:RNA, Small Interfering / Q000378:metabolism; D016601:RNA-Binding Proteins / Q000378:metabolism*; D050796:STAT3 Transcription Factor / Q000378:metabolism*; D015398:Signal Transduction; D000071222:Suppressor of Cytokine Signaling 1 Protein / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D001057:Apolipoproteins E; D051017:Apoptosis Regulatory Proteins; D035683:MicroRNAs; C532623:Mirn155 microRNA, mouse; C498443:Pdcd4 protein, mouse; D034741:RNA, Small Interfering; D016601:RNA-Binding Proteins; D050796:STAT3 Transcription Factor; C491590:Socs1 protein, mouse; C494087:Stat3 protein, mouse; D000071222:Suppressor of Cytokine Signaling 1 Protein; D014409:Tumor Necrosis Factor-alpha