CAJ | 학술논문

目的探讨细胞因子信号转导抑制因子3( SOCS3)抑制血管平滑肌细胞炎症反应的作用及机制.方法用携带大鼠SOCS3基因的腺病毒(pYrAd-rSOCS3)转染血小板衍生生长因子-BB(PDGF-BB)刺激的大鼠动脉血管平滑肌细胞.实时定量聚合酶链反应(Real time-PCR)检测SOCS3、白细胞介素(IL) -1β、IL-6、肿瘤坏死因子(TNF)-α、单核细胞趋化蛋白-1(MCP-1)及细胞间黏附分子-1(ICAM-1)mRNA表达.Western blot检测SOCS3、信号转导及转录激活因子3(STAT3)、P-STAT3、IL-1β、IL-6、TNF-α、MCP-1及ICAM-1的的蛋白表达.结果 PDGF-BB刺激血管平滑肌细胞24h后,SOCS3、STAT3、P-STAT3、IL-1β、IL-6、TNF-α、MCP-1及ICAM-1表达均上调；pYrAd-rSOCS3转染血管平滑肌细胞后再用PDGF-BB刺激,其SOCS3表达进一步上调,但STAT3、P-STAT3、IL-1β、IL-6、TNF-α、MCP-1及ICAM-1表达明显下调.结论上调血管平滑肌细胞SOCS3表达通过负反馈调节酪氨酸蛋白激酶(JAK) -STAT3信号通路,抑制STAT3的激活及磷酸化而下调炎性细胞因子表达.
목적 탐토세포인자신호전도억제인자3( SOCS3)억제혈관평활기세포염증반응적작용급궤제.방법 용휴대대서SOCS3기인적선병독(pYrAd-rSOCS3)전염혈소판연생생장인자-BB(PDGF-BB)자격적대서동맥혈관평활기세포.실시정량취합매련반응(Real time-PCR)검측SOCS3、백세포개소(IL) -1β、IL-6、종류배사인자(TNF)-α、단핵세포추화단백-1(MCP-1)급세포간점부분자-1(ICAM-1)mRNA표체.Western blot검측SOCS3、신호전도급전록격활인자3(STAT3)、P-STAT3、IL-1β、IL-6、TNF-α、MCP-1급ICAM-1적적단백표체.결과 PDGF-BB자격혈관평활기세포24h후,SOCS3、STAT3、P-STAT3、IL-1β、IL-6、TNF-α、MCP-1급ICAM-1표체균상조；pYrAd-rSOCS3전염혈관평활기세포후재용PDGF-BB자격,기SOCS3표체진일보상조,단STAT3、P-STAT3、IL-1β、IL-6、TNF-α、MCP-1급ICAM-1표체명현하조.결론 상조혈관평활기세포SOCS3표체통과부반궤조절락안산단백격매(JAK) -STAT3신호통로,억제STAT3적격활급린산화이하조염성세포인자표체.
Objective To investigate the inhibitory effect of suppressor of cytokine signaling3 (SOCS3) on the pro-inflammation of platelet-derived growth factor-BB (PDGF-BB)-induced vascular smooth muscle cells (VSMCs).Methods The recombinant adenovirus vector containing rat SOCS3 gene was transfected into VSMCs induced by PDGF-BB.After 24 h,real-time reverse transcription polymerase chain reaction (RT-PCR) and Western blotting were used to analyse the mRNA and protein expression of SOCS3,signal transducer and activators of transcription 3 (STAT3) ( only by Western blotting),P-STAT3 ( only by Western blotting),interleukin (IL) -1 β,IL-6,tumor necrosis factor (TNF) -α,monocyte chemoattractant protein (MCP)-1 and intercellular adhesion molecule-1 (ICAM-1).Results The expression levels of SOCS3 mRNA and protein,STAT3 protein,P-STAT3 protein,IL-1 β,IL-6,TNF-α,MCP-1 and ICAM-1 were significantly up-regulated in VSMCs induced by PDGF-BB.However,after VSMCs were transfected with pYrAd-rSOCS3 and treated with PDGF-BB,the expression of SOCS3 mRNA and protein was further up-regulated,and that of STAT3 protein,P-STAT3 protein,IL-1 β,IL-6,TNF-α,MCP-1 and ICAM-1 was significantly down-regulated.Conclusion In VSMCs,up-regulated SOCS3 may inhibit proinflammatory effect of VSMCs by blocking STAT3 activation and phosphorylation through negatively regulating JAK-STAT3 signaling pathway.These results can provide a novel idea for clinical treatment of vascular proliferation diseases.