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The LncRNA H19/miR-1-3p/CCL2 axis modulates lipopolysaccharide (LPS) stimulation-induced normal human astrocyte proliferation and activation
Cytokine ( IF 3.8 ) Pub Date : 2020-07-01 , DOI: 10.1016/j.cyto.2020.155106
Pengzhi Li 1 , Yawei Li 1 , Yuliang Dai 1 , Bing Wang 1 , Lei Li 1 , Bin Jiang 1 , Pengfei Wu 2 , Jietao Xu 1
Affiliation  

Reactive astrocyte proliferation post SCI (spinal cord injury) leads to the formation of glial scars, thus hindering axon regeneration and SCI repair, during which the activation of astrocytes plays a central role. This study attempted to identify the lncRNA-miRNA-mRNA network which exerts a critical effect on normal human astrocyte (NHA) activation and proliferation during SCI inflammation. Herein, lncRNA H19 expression was increased by LPS in NHAs, and H19 was positively correlated with CCL2. H19 silencing in NHAs significantly attenuated the promoting effects of LPS stimulation on NHA proliferation and activation as manifested by inhibited cell viability and DNA synthesis capacity, reduced NHA activation markers, and reduced inflammatory factor concentrations (CCL2, IL-6, and TNF-α). miR-1-3p directly bound to H19 and the CCL2 3'UTR. miR-1-3p overexpression also attenuated the promoting effects of LPS stimulation on NHA proliferation and activation. H19 relieved miR-1-3p-induced inhibition of CCL2 expression by acting as a ceRNA. The inhibition of miR-1-3p could significantly reverse the effects of H19 silencing on NHA proliferation and activation, suggesting that the H19/miR-1-3p axis regulates the proliferation and activation of NHAs via CCL2. In conclusion, lncRNA H19, miR-1-3p, and CCL2 form a lncRNA-miRNA-mRNA axis that modulates NHA proliferation and activation in vitro.

中文翻译:

LncRNA H19/miR-1-3p/CCL2 轴调节脂多糖 (LPS) 刺激诱导的正常人星形胶质细胞增殖和激活

SCI(脊髓损伤)后反应性星形胶质细胞增殖导致胶质瘢痕形成,从而阻碍轴突再生和 SCI 修复,在此期间星形胶质细胞的激活起着核心作用。本研究试图确定 lncRNA-miRNA-mRNA 网络,该网络在 SCI 炎症期间对正常人星形胶质细胞 (NHA) 的激活和增殖发挥关键作用。在此,lncRNA H19 表达在 NHA 中被 LPS 增加,并且 H19 与 CCL2 呈正相关。NHA 中的 H19 沉默显着减弱了 LPS 刺激对 NHA 增殖和激活的促进作用,表现为细胞活力和 DNA 合成能力受到抑制,NHA 激活标志物减少,炎症因子浓度(CCL2、IL-6 和 TNF-α)降低. miR-1-3p 直接与 H19 和 CCL2 3'UTR 结合。miR-1-3p 过表达也减弱了 LPS 刺激对 NHA 增殖和活化的促进作用。H19 通过充当 ceRNA 解除了 miR-1-3p 诱导的 CCL2 表达抑制。抑制 miR-1-3p 可以显着逆转 H19 沉默对 NHA 增殖和激活的影响,表明 H19/miR-1-3p 轴通过 CCL2 调节 NHA 的增殖和激活。总之,lncRNA H19、miR-1-3p和CCL2形成lncRNA-miRNA-mRNA轴,在体外调节NHA增殖和活化。抑制 miR-1-3p 可以显着逆转 H19 沉默对 NHA 增殖和激活的影响,表明 H19/miR-1-3p 轴通过 CCL2 调节 NHA 的增殖和激活。总之,lncRNA H19、miR-1-3p和CCL2形成lncRNA-miRNA-mRNA轴,在体外调节NHA增殖和活化。抑制 miR-1-3p 可以显着逆转 H19 沉默对 NHA 增殖和激活的影响,表明 H19/miR-1-3p 轴通过 CCL2 调节 NHA 的增殖和激活。总之,lncRNA H19、miR-1-3p和CCL2形成lncRNA-miRNA-mRNA轴,在体外调节NHA增殖和活化。
更新日期:2020-07-01
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