Circular RNA expression in isoproterenol hydrochloride-induced cardiac hypertrophy

Circular RNA (circRNA) is a novel class of noncoding RNAs, and the roles of circRNAs in the development of cardiac hypertrophy remain to be explored. Here, we investigate the potential roles of circRNAs in cardiac hypertrophy. By circRNA sequencing in left ventricular specimens collected from 8-week...

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Veröffentlicht in:Aging (Albany, NY.) NY.), 2020-02, Vol.12 (3), p.2530-2544
Hauptverfasser: Yang, Ming-Hui, Wang, Hao, Han, Sheng-Na, Jia, Xin, Zhang, Si, Dai, Fei-Fei, Zhou, Meng-Jiao, Yin, Zhongnan, Wang, Tian-Qi, Zang, Ming-Xi, Xue, Li-Xiang
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Sprache:eng
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Zusammenfassung:Circular RNA (circRNA) is a novel class of noncoding RNAs, and the roles of circRNAs in the development of cardiac hypertrophy remain to be explored. Here, we investigate the potential roles of circRNAs in cardiac hypertrophy. By circRNA sequencing in left ventricular specimens collected from 8-week-old mice with isoproterenol hydrochloride-induced cardiac hypertrophy, we found 401 out of 3323 total circRNAs were dysregulated in the hypertrophic hearts compared with the controls. Of these, 303 circRNAs were upregulated and 98 were downregulated. Moreover, the GO and KEGG analyses revealed that the majority of parental gene of differentially expressed circRNAs were not only related to biological process such as metabolic process and response to stimulus, but also related to pathway such as circulatory system and cardiovascular diseases. On the other hand, total 1974 miRNAs were predicted to binding to these differentially expressed circRNAs, and the possible target mRNAs of those miRNAs were also predicted and analyzed in terms of functional annotation. Finally, we identified that ANF and miR-23a are downstream targets of circRNA wwp1, suggesting that circRNA wwp1 exerts inhibitory roles of cardiac hypertrophy via down-regulation of ANF and miR-23a, which underlying the potential mechanisms whereby circRNA regulates cardiac hypertrophy.
ISSN:1945-4589
1945-4589
DOI:10.18632/aging.102761