IMR Press / FBL / Volume 21 / Issue 2 / DOI: 10.2741/4393

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Article

Mir-27a promotes apoptosis of cochlear sensory epithelium in Cx26 knockout mice

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1 Department of Otorhinolaryngology, Affiliated Eye and ENT Hospital of Fudan University, Shanghai 200031, China
2 Center Clinical Laboratory, Children’s Hospital of Fudan University, Shanghai 201102, China
Academic Editor:Fei He
Front. Biosci. (Landmark Ed) 2016, 21(2), 364–373; https://doi.org/10.2741/4393
Published: 1 January 2016
(This article belongs to the Special Issue Cellular immunology and stem cell biology)
Abstract

To investigate the underlying molecular mechanism for connexin 26 (Cx26) knockout-induced apoptosis, we performed TUNEL assays to detect apoptosis in the cochlear sensory epithelium in Cx26 knockout mice. We also compared the miRNA expression profiles of Cx26 knockout and wild-type mice using microarray technology and bioinformatic analyses. Real-time PCR, luciferase reporter gene assays, and scala media microinjections were performed to identify the effect of a specific miRNA and its targets. The results showed that apoptosis increased in the cochlear sensory epithelium of Cx26 knockout mice. The abnormal expression of mir-27a and sgk1 in Cx26 knockout mice was verified with real-time PCR. Luciferase reporter gene assays showed that overexpression of mir-27a significantly decreased sgk1 reporter gene activity; an inhibitor of mir-27a blocked the effect. Mir-27a lentivirus also inhibited sgk1 expression in cultured cochlear tissue. Mir-27a shRNA treatment inhibited Cx26 knockout-induced apoptosis in the cochlear sensory epithelium of mice and increased the expression of sgk1 mRNA. Thus, mir-27a was identified as an apoptotic molecule that participates in Cx26 knockout-induced apoptosis in the cochlear sensory epithelium of mice by downregulating sgk1 expression.

Keywords
Apoptosis
Connexin26
Cochlear Sensory Epithelium
mir-27a
sgk1
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