Department of Cardiac Intervention, Linyi People's Hospital, Linyi 276000, Shandong, China.
Department of Critical Care Medicine, Aerospace Center Hospital, Haidian, 100049, Beijing, China.
Aging (Albany NY). 2020 Jun 6;12(11):10441-10456. doi: 10.18632/aging.103269.
Previous studies have shown that lncRNA small nuclear RNA host gene 7 (lncRNA SNHG7) played an important role in cancer progression. However, the role of lncRNA SNHG7 in cardiac fibrosis is still poorly understood. In this study, the results of quantitative real time polymerase chain reaction (qRT-PCR) analysis showed that lncRNA SNHG7 was over expressed in the infarcted and peri-infarcted area in the left ventricle after MI in mice. Western blot analysis showed that knockdown of SNHG7 decreased the expression of collagen type 1 (Col1)and α-smooth muscle actin (α-SMA). Echocardiographic study suggested that inhibition of SNHG7 improved cardiac function after MI in mice. Luciferase assay indicated SNHG7 could act as a competing endogenous RNA (ceRNA) by sponging miR-34-5p. The MTT cell proliferation assay and 5-ethynyl-2'-deoxyuridine (EdU) labelling assay revealed that co-transfection of SNHG7 and miR-34-5p inhibited cell viability and proliferation of cardiac fibroblasts (CF). All the results indicated that lncRNA SNHG7 could promote cardiac fibrosis via targeting miR-34-5p through acting as a ceRNA in mice after MI. Silencing of SNHG7 could attenuate deposition of collagens and improve cardiac function. miR-34-5p could suppress the fibrogenesis of CF by targeting ROCK1 and abolish SNHG7-induced CF proliferation and fibroblast-to-myofibroblast transition.
先前的研究表明，长非编码 RNA 小核 RNA 宿主基因 7（lncRNA SNHG7）在癌症进展中发挥重要作用。然而，lncRNA SNHG7 在心脏纤维化中的作用仍知之甚少。在这项研究中，定量实时聚合酶链反应（qRT-PCR）分析的结果表明，lncRNA SNHG7 在小鼠心肌梗死后左心室梗死和梗死周围区域过度表达。Western blot 分析表明，SNHG7 的敲低降低了胶原 I（Col1）和α-平滑肌肌动蛋白（α-SMA）的表达。超声心动图研究表明，抑制 SNHG7 可改善小鼠心肌梗死后的心功能。荧光素酶测定表明，SNHG7 可通过海绵 miR-34-5p 作为竞争内源性 RNA（ceRNA）发挥作用。MTT 细胞增殖试验和 5-乙炔基-2'-脱氧尿苷（EdU）标记试验表明，SNHG7 和 miR-34-5p 的共转染抑制了心脏成纤维细胞（CF）的活力和增殖。所有结果表明，lncRNA SNHG7 可通过作为 ceRNA 靶向 miR-34-5p 促进 MI 后小鼠的心脏纤维化。沉默 SNHG7 可减少胶原沉积并改善心功能。miR-34-5p 可通过靶向 ROCK1 抑制 CF 的纤维化，并消除 SNHG7 诱导的 CF 增殖和纤维母细胞向肌成纤维细胞转化。
