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MiR‐204 promotes apoptosis in oxidative stress‐induced rat Schwann cells by suppressing neuritin expression
Author(s) -
Gao Rui,
Wang Liming,
Sun Jun,
Nie Kun,
Jian Huiling,
Gao Lei,
Liao Xinhua,
Zhang Haiyuan,
Huang Jin,
Gan Shangquan
Publication year - 2014
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2014.07.004
Subject(s) - microbiology and biotechnology , apoptosis , microrna , schwann cell , oxidative stress , neurotrophin , biology , chemistry , gene , biochemistry , receptor
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 H 2 O 2 ‐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.