Long Noncoding RNA HOTAIR Functions as a Competitive Endogenous RNA to Regulate Connexin43 Remodeling in Atrial Fibrillation by Sponging MicroRNA-613.
Long Noncoding RNA HOTAIR Functions as a Competitive Endogenous RNA to Regulate Connexin43 Remodeling in Atrial Fibrillation by Sponging MicroRNA-613.
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长非编码 RNA HOTAIR 作为竞争性内源性 RNA 通过海绵 MicroRNA-613 调节心房颤动中的 Connexin43 重塑
DOI：
10.1155/2020/5925342
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发表时间：
2020
影响因子：
3.1
通讯作者：
Jiang Z
中科院分区：
文献类型：
--
作者：
Dai W;Chao X;Li S;Zhou S;Zhong G;Jiang Z
多项研究表明，长非编码RNA（lncRNA）-HOX转录反义RNA（HOTAIR）作为竞争性内源RNA（ceRNA）调节基因表达，从而参与一些心血管疾病。编码 Cx43 的 GJA1 是 microRNA-613 (miR-613) 的一种潜在靶基因。同时，HOTAIR与miR-613之间存在潜在的靶点调控关系。本研究旨在研究 HOTAIR 是否作为 ceRNA 通过海绵 miR-613 来调节心房颤动 (AF) 中 Cx43 的表达。在 45 例心脏瓣膜疾病患者（其中 23 例慢性 AF 患者）的右心耳中检测到 HOTAIR、miR-613 和 Cx43 的表达。构建HOTAIR过表达和低表达的HL-1细胞模型以证实HOTAIR对Cx43的作用。然后，共转染HOTAIR和miR-613后，检测Cx43表达以证明HOTAIR和miR-613之间的相互作用。此外，进行荧光素酶测定以验证 HOTAIR 可以通过海绵 miR-613 来调节 Cx43 重塑为 ceRNA。慢性AF组HOTAIR和Cx43的表达显着下调。 HOTAIR 正向调节 HL-1 细胞中 Cx43 的表达。 HOTAIR 对 Cx43 表达的上调作用可以被 miR-613 显着减弱。此外，HOTAIR可明显减轻miR-613对Cx43表达的抑制作用。最后，荧光素酶测定证实 HOTAIR 通过海绵 miR-613 在 Cx43 表达中发挥 ceRNA 的作用。我们的研究表明，HOTAIR 通过海绵 miR-613 作为 ceRNA 发挥作用，是 AF 中 Cx43 重塑的重要贡献者。
Several studies have indicated that long noncoding RNAs (lncRNAs)-HOX transcript antisense RNA (HOTAIR) is involved in some cardiovascular diseases by regulating gene expression as a competitive endogenous RNA (ceRNA). GJA1 encoding Cx43 is one potential target gene of microRNA-613 (miR-613). Meanwhile, there is a potential target regulatory relationship between HOTAIR and miR-613. The present study is aimed at investigating whether HOTAIR functions as a ceRNA to regulate the Cx43 expression in atrial fibrillation (AF) by sponging miR-613. The expressions of HOTAIR, miR-613, and Cx43 were detected in the right atrial appendages of 45 patients with heart valve disease, including 23 patients with chronic AF. The HOTAIR overexpressed and underexpressed HL-1 cell model were constructed to confirm the effect of HOTAIR on Cx43. Then, the Cx43 expression was detected to testify the interplay between HOTAIR and miR-613 after cotransfecting HOTAIR and miR-613. Furthermore, luciferase assays were performed to verify that HOTAIR could regulate Cx43 remolding as a ceRNA by sponging miR-613. The expression of HOTAIR and Cx43 was significantly downregulated in chronic AF group. HOTAIR regulated positively the Cx43 expression in HL-1 cells. The upregulated effect of HOTAIR on the Cx43 expression could be remarkably attenuated by miR-613. Moreover, the inhibitory effect of miR-613 on the Cx43 expression could be obviously mitigated by HOTAIR. At last, luciferase assays confirmed HOTAIR functioned as a ceRNA in the Cx43 expression by sponging miR-613. Our study suggests that HOTAIR, functioning as a ceRNA by sponging miR-613, is an important contributor to Cx43 remolding in AF.
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影响因子：
7.4
作者：
Greco S;Zaccagnini G;Perfetti A;Fuschi P;Valaperta R;Voellenkle C;Castelvecchio S;Gaetano C;Finato N;Beltrami AP;Menicanti L;Martelli F
通讯作者：
Martelli F
影响因子：
37.8
作者：
Igarashi T;Finet JE;Takeuchi A;Fujino Y;Strom M;Greener ID;Rosenbaum DS;Donahue JK
通讯作者：
Donahue JK
影响因子：
8
作者：
Peng WX;Koirala P;Mo YY
通讯作者：
Mo YY
影响因子：
37.8
作者：
HENRY, WL;MORGANROTH, J;EPSTEIN, SE
通讯作者：
EPSTEIN, SE
影响因子：
3.4
作者：
Chen, Guiying;Guo, Hong;Liu, Chang
通讯作者：
Liu, Chang