NDLI: Mst3b Promotes Spinal Cord Neuronal Regeneration by Promoting Growth Cone Branching Out in Spinal Cord Injury Rats

Content Provider	Springer Nature Link
Author	Zhang, Yuqiang Hu, Huaiqiang Tian, Ting Zhang, Luping Zhao, Dongmei Wu, Qianqian Chang, Yingwei Wang, Qingbo Zhou, Shuai Feng, Guoying Huang, Fei
Copyright Year	2014
Abstract	Spinal cord injury is a severe clinical problem, and research searching activity molecular that can promote spinal cord injury repairing is very prevalent. Mst3b can promote repair of damaged peripheral nerves and the optic nerve, but has been rarely reported in spinal cord injury research. Through detecting its expression in different periods of injured spinal cord, we found that the expression of Mst3b was significantly upregulated in injured spinal cord neurons. Increasing Mst3b expression using adenovirus in vivo and in vitro promoted axonal regeneration of spinal cord neurons, which led to behavioral and electrophysiological improvement. Downregulation of Mst3b level had the adverse effects. Increasing Mst3b expression in PC12 cells resulted in an elevation of P42/44$^{MAPK}$ and LIMK/Cofilin activation. These results identified Mst3b as a powerful regulator for promoting spinal cord injury recovery through the P42/44$^{MAPK}$ and LIMK/Cofilin signaling pathways.
Starting Page	1144
Ending Page	1157
Page Count	14
File Format	PDF
ISSN	08937648
Journal	Molecular Neurobiology
Volume Number	51
Issue Number	3
e-ISSN	15591182
Language	English
Publisher	Springer US
Publisher Date	2014-07-03
Publisher Place	New York
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Mst3b Spinal cord injury (SCI) Neural regeneration Small G protein Actin Growth cone Neurosciences Neurobiology Cell Biology Neurology
Content Type	Text
Resource Type	Article
Subject	Neurology Cellular and Molecular Neuroscience

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

Autophagy Reduces Neuronal Damage and Promotes Locomotor Recovery via Inhibition of Apoptosis After Spinal Cord Injury in Rats

Heme oxygenase-1 promotes neuron survival through down-regulation of neuronal NLRP1 expression after spinal cord injury

BET protein inhibition regulates cytokine production and promotes neuroprotection after spinal cord injury

Epidermal growth factor receptor inhibitor ameliorates excessive astrogliosis and improves the regeneration microenvironment and functional recovery in adult rats following spinal cord injury

Erratum to: Autophagy Reduces Neuronal Damage and Promotes Locomotor Recovery via Inhibition of Apoptosis after Spinal Cord Injury in Rats

Valproic Acid Arrests Proliferation but Promotes Neuronal Differentiation of Adult Spinal NSPCs from SCI Rats

HMGB1 Contributes to Regeneration After Spinal Cord Injury in Adult Zebrafish

Neutrophil contribution to spinal cord injury and repair

Apelin alleviated neuroinflammation and promoted endogenous neural stem cell proliferation and differentiation after spinal cord injury in rats

Mst3b Promotes Spinal Cord Neuronal Regeneration by Promoting Growth Cone Branching Out in Spinal Cord Injury Rats

Similar Documents

Autophagy Reduces Neuronal Damage and Promotes Locomotor Recovery via Inhibition of Apoptosis After Spinal Cord Injury in Rats

Heme oxygenase-1 promotes neuron survival through down-regulation of neuronal NLRP1 expression after spinal cord injury

BET protein inhibition regulates cytokine production and promotes neuroprotection after spinal cord injury

Epidermal growth factor receptor inhibitor ameliorates excessive astrogliosis and improves the regeneration microenvironment and functional recovery in adult rats following spinal cord injury

Erratum to: Autophagy Reduces Neuronal Damage and Promotes Locomotor Recovery via Inhibition of Apoptosis after Spinal Cord Injury in Rats

Valproic Acid Arrests Proliferation but Promotes Neuronal Differentiation of Adult Spinal NSPCs from SCI Rats

HMGB1 Contributes to Regeneration After Spinal Cord Injury in Adult Zebrafish

Neutrophil contribution to spinal cord injury and repair

Apelin alleviated neuroinflammation and promoted endogenous neural stem cell proliferation and differentiation after spinal cord injury in rats

Mst3b Promotes Spinal Cord Neuronal Regeneration by Promoting Growth Cone Branching Out in Spinal Cord Injury Rats