miR-30b Promotes spinal cord sensory function recovery via the Sema3A/NRP-1/PlexinA1/RhoA/ROCK Pathway

被引：19

作者：

Wang, Xin ^{[1
]}

Li, Bo ^{[2
]}

Wang, Zhijie ^{[3
]}

Wang, Fengyan ^{[4
]}

Liang, Jing ^{[5
]}

Chen, Chuanjie ^{[6
]}

Zhao, Lei ^{[7
]}

Zhou, Bo ^{[1
,8
]}

Guo, Xiaoling ^{[8
]}

Ren, Liqun ^{[9
]}

Yuan, Xin ^{[10
]}

Chen, Xueming ^{[10
]}

Wang, Tianyi ^{[4
]}

机构：

[1] Chengde Med Univ, Chengde, Peoples R China

[2] Sun Yat Sen Univ, Sun Yat Sen Mem Hosp, Dept Orthoped, Guangzhou, Peoples R China

[3] Chengde Med Univ, Affiliated Hosp, Dept Pediat Internal Med, Chengde, Peoples R China

[4] 981st Hosp Chinese Peoples Liberat Army Joint Log, Dept Orthoped, Chengde 067000, Hebei, Peoples R China

[5] 981st Hosp Chinese Peoples Liberat Army Joint Log, Dept Nursing, Chengde, Peoples R China

[6] Chengde Cent Hosp, Dept Orthoped, Chengde, Peoples R China

[7] Chengde Med Univ, Affiliated Hosp, Dept Educ, Chengde, Peoples R China

[8] 981st Hosp Chinese Peoples Liberat Army Joint Log, Dept Neurol, Chengde 067000, Hebei, Peoples R China

[9] Chengde Med Univ, Lab Spinal Cord Injury & Rehabil, Chengde, Peoples R China

[10] Capital Med Univ, Beijing Luhe Hosp, Dept Spine Surg, Beijing 100020, Peoples R China

来源：

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE | 2020年 / 24卷 / 21期

关键词：

miR-30b; primary sensory neuron; RhoA; sema3A; spinal cord injury; NEUROPATHIC PAIN; PARKINSONS-DISEASE; INJURY; INDIVIDUALS; EXPRESSION; OUTGROWTH; GROWTH; CELLS;

D O I：

10.1111/jcmm.15591

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

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.

引用

页码：12285 / 12297

页数：13

共 48 条

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