CircERBB2IP promotes post-infarction revascularization via the miR-145a-5p/Smad5 axis.
CircERBB2IP promotes post-infarction revascularization via the miR-145a-5p/Smad5 axis.
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CircERBB2IP 通过 miR-145a-5p/Smad5 轴促进梗死后血运重建
DOI：
10.1016/j.omtn.2022.04.006
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发表时间：
2022-06-14
期刊：
影响因子：
--
通讯作者：
Shi, Bei
中科院分区：
文献类型：
--
作者：
Long, Xianping;Qiu, Zhimei;Li, Chaofu;Wang, Yan;Li, Jiao;Zhao, Ranzun;Rong, Jidong;Gu, Ning;Yuan, Jinson;Ge, Junbo;Shi, Bei
心肌梗死是世界范围内导致死亡和残疾的主要疾病之一，损伤组织的血运重建是心肌损伤修复的关键。CircRNAs(CircRNAs)广泛参与全身各系统的生理和病理过程，其在心血管疾病中的作用日益受到重视。在这项研究中，我们确定了大约ERBB2IP在新生小鼠的心脏中高度表达。在体内和体外，沉默或过表达CircERBB2IP分别抑制和促进血管生成。在机制上，转录因子GATA4促进大约ERBB2IP的产生。此外，CircERBB2IP作为内源性miR-145a-5p的海绵，能够隔离和抑制miR-145a-5p的活性，从而导致Smad5的表达水平增加。综上所述，ERBB2IP可通过miR-145a-5p/Smad5轴促进心肌梗死后血管生成。提示ERBB2IP可能是治疗心肌梗死的潜在靶点。CircBB2IP在新生小鼠心脏中高表达，并随着心脏发育逐渐降低。CircERBB2IP在体内和体外促进CMECs的增殖、迁移和管状形成。从机制上讲，ERBB2IP通过ERBB2IP/miR-145a-5p/Smad5轴介导血管生成。
Myocardial infarction is one of the leading diseases causing death and disability worldwide, and the revascularization of damaged tissues is essential for myocardial-injury repair. Circular RNAs (circRNAs) are widely involved in physiological and pathological processes in various systems throughout the body, and the role of circRNAs in cardiovascular disease is gaining attention. In this study, we determined that circERBB2IP is highly expressed in the hearts of newborn mice. Silencing or overexpression of circERBB2IP inhibited and promoted angiogenesis in vivo and in vitro, respectively. Mechanistically, the transcription factor GATA4 promotes the production of circERBB2IP. Furthermore, circERBB2IP functioned as an endogenous miR-145a-5p sponge and was able to sequester and repress miR-145a-5p activity, which led to an increased expression level of Smad5. In summary, circERBB2IP can promote angiogenesis after myocardial infarction through the miR-145a-5p/Smad5 axis. These data suggest that circERBB2IP may be a potential therapeutic target for the treatment of myocardial infarction. circERBB2IP was highly expressed in newborn mice hearts, and its level gradually decreased with cardiac development. circERBB2IP promotes proliferation, migration, and tube formation of CMECs in vivo and in vitro. Mechanistically, circERBB2IP mediates angiogenesis through the circERBB2IP/miR-145a-5p/Smad5 axis.
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