Open Access

ΜicroRNA‑155 induces protection against cerebral ischemia/reperfusion injury through regulation of the Notch pathway in vivo

  • Authors:
    • Tianpeng Jiang
    • Shi Zhou
    • Xing Li
    • Jie Song
    • Tianzhi An
    • Xueqin Huang
    • Xiuqin Ping
    • Lizhou Wang
  • View Affiliations

  • Published online on: May 17, 2019     https://doi.org/10.3892/etm.2019.7590
  • Pages: 605-613
  • Copyright: © Jiang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

microRNA (miR)‑155 has been demonstrated to participate in the regulation of endothelium during cerebral ischemia. In the present study, it was aimed to investigate the molecular mechanism of miR‑155 in the regulation of cerebral ischemia/reperfusion (I/R) injury with middle cerebral artery occlusion (MCAO) in mice. The MCAO model was established in C57BL/6 mice. Transfection of miR‑155 mimics and miR‑155 inhibitors was performed to alter the expression of miR‑155. The level of miR‑155 was measured by RT‑qPCR analysis. The western blotting results demonstrated that deletion of miR‑155 increased the expression of Notch1, intracellular Notch receptor domain (NICD) and hairy and enhancer of split‑1 (Hes1) levels. In addition, the percentage of terminal deoxynucleotidyl‑transferase‑mediated dUTP nick end labeling‑positive cells and caspase‑3 levels were decreased following treatment with a miR‑155 inhibitor compared with the Pre‑IR group. Notably, disrupting miR‑155 also increased nitric oxide (NO) production and the expression of endothelial NO synthase (eNOS), leading to downregulation of brain water content and Evans blue levels. However, overexpression of miR‑155 restored all these changes to similar levels observed in the cerebral I/R injury group. The expressions of Notch1, NICD and Hes1 were also decreased to the cerebral I/R injury condition. In conclusion, a novel mechanism was identified for abrogating normal NO production and eNOS expression via the aberrant expression of the Notch signaling pathway, a mechanism that may be modulated by miR‑155. Together, these results reveal important functions of miR‑155 in regulating the Notch signaling pathway of the nervous system, and a potential role for miR‑155 as a crucial therapy target for cerebral stroke.
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July-2019
Volume 18 Issue 1

Print ISSN: 1792-0981
Online ISSN:1792-1015

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Spandidos Publications style
Jiang T, Zhou S, Li X, Song J, An T, Huang X, Ping X and Wang L: ΜicroRNA‑155 induces protection against cerebral ischemia/reperfusion injury through regulation of the Notch pathway in vivo. Exp Ther Med 18: 605-613, 2019.
APA
Jiang, T., Zhou, S., Li, X., Song, J., An, T., Huang, X. ... Wang, L. (2019). ΜicroRNA‑155 induces protection against cerebral ischemia/reperfusion injury through regulation of the Notch pathway in vivo. Experimental and Therapeutic Medicine, 18, 605-613. https://doi.org/10.3892/etm.2019.7590
MLA
Jiang, T., Zhou, S., Li, X., Song, J., An, T., Huang, X., Ping, X., Wang, L."ΜicroRNA‑155 induces protection against cerebral ischemia/reperfusion injury through regulation of the Notch pathway in vivo". Experimental and Therapeutic Medicine 18.1 (2019): 605-613.
Chicago
Jiang, T., Zhou, S., Li, X., Song, J., An, T., Huang, X., Ping, X., Wang, L."ΜicroRNA‑155 induces protection against cerebral ischemia/reperfusion injury through regulation of the Notch pathway in vivo". Experimental and Therapeutic Medicine 18, no. 1 (2019): 605-613. https://doi.org/10.3892/etm.2019.7590