Open AccessmiR‐30b Promotes spinal cord sensory function recovery via the Sema3A/NRP‐1/PlexinA1/RhoA/ROCK Pathway
Author(s) -
Wang Xin,
Li Bo,
Wang Zhijie,
Wang Fengyan,
Liang Jing,
Chen Chuanjie,
Zhao Lei,
Zhou Bo,
Guo Xiaoling,
Ren Liqun,
Yuan Xin,
Chen Xueming,
Wang Tianyi
Publication year - 2020
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.15591
Subject(s) - sema3a , rhoa , neurite , semaphorin , growth cone , microbiology and biotechnology , inhibitory postsynaptic potential , downregulation and upregulation , spinal cord , chemistry , neuroscience , biology , axon , signal transduction , biochemistry , in vitro , receptor , gene
Spinal cord injury (SCI) induces both motor and sensory dysfunctions. We wondered whether miR‐30b could promote primary sensory neuron (PSN) axon growth in inhibitory microenvironment. The neurite growth was promoted by miR‐30b agomir and inhibited by antagomir. MiR‐30b targeted and degraded sema3A mRNA. MiR‐30b regulated the formation of sema3A‐NRP‐1‐PlexinA1 complex via targeting sema3A. The neurite length was induced by the miR‐30b agomir, and the application of sema3A protein could reverse the effect of agomir. GTP‐RhoA and ROCK expression were down‐regulated by miR‐30b. Neurite outgrowth that inhibited by sema3A and the miR‐30b antagomir was increased by Y‐27632. Agomir promoted neurite growth in NogoA inhibitory conditions, which indicated miR‐30b could both enhance neuronal intrinsic regenerative ability and promote neurite growth against inhibitory microenvironment via Sema3A/NRP‐1/PlexinA1/RhoA/ROCK axis. The agomir could also regulate Sema3A/NRP‐1/PlexinA1/RhoA/ROCK axis in vivo and restore spinal cord sensory conductive function. In conclusion, miR‐30b could be a novel target for sensation recovery after SCI.