MiR‐204 promotes apoptosis in oxidative stress‐induced rat Schwann cells by suppressing neuritin expression. Issue 17 (15th July 2014)

• Record Type: Journal Article
• Authors: Gao, Rui; Wang, Liming; Sun, Jun; Nie, Kun; Jian, Huiling; Gao, Lei; Liao, Xinhua; Zhang, Haiyuan; Huang, Jin; Gan, Shangquan
• Is Part Of: FEBS letters. Volume 588:Issue 17(2014)
• Page Start: 3225
• Page End: 3232
• Publication Date: 2014-07-15
• Subjects: MicroRNA -- Neuritin -- Nerve injury and repair -- Apoptosis; Biochemistry -- Periodicals; Biophysics -- Periodicals; Molecular biology -- Periodicals; Biochimie -- Périodiques; Biochemistry; Biophysics; Molecular biology; Periodicals; 572.05
• DOI: 10.1016/j.febslet.2014.07.004
• Languages: English
• ISSNs: 0014-5793

Abstract

Abstract : Neuritin ( Nrn1 ) is a neurotrophin that plays an important role in nervous system plasticity and repair following nerve injury. MicroRNAs (miRNAs) are a type of small non‐coding RNA that regulate nearly all aspects of nerve development and survival, including apoptosis. Here it was found that miR‐204 negatively regulates Nrn1 protein expression through direct interaction with Nrn1 transcript. Moreover, miR‐204 activates cleaved caspase‐3, enhancing the sensitivity of RSC96 Schwann cells to H2 O2 ‐induced oxidative stress and apoptosis. Thus, miR‐204 expressed at a low level may create a microenvironment suitable for the repair of injured nerves by relieving the inhibition of Nrn1 transcription and stimulating the anti‐apoptotic function of Schwann cells. These results provide novel insights into the roles of miR‐204 in nerve injury and repair. Abstract : The expression pattern of miR‐204 inversely correlated with the expression change of Nrn1 during nerve repair of TGI model. It is the first time to report that Nrn1 is a direct target and can be down‐regulated by miR‐204 in vitro and in vivo. MiR‐204 can stimulate apoptosis of oxidative stress‐induced Schwann cells. Low expression of miR‐204 may contribute to create a suitable microenvironment for the repair of injured nerves.