NDLI: An Upregulation of SENP3 After Spinal Cord Injury: Implications for Neuronal Apoptosis

Content Provider	Springer Nature Link
Author	Wei, Haixiang Teng, Honglin Huan, Weipeng Zhang, Shuangwei Fu, Hongran Chen, Fangyi Wang, Jing Wu, Chunlei Zhao, Jian
Copyright Year	2012
Abstract	SENP3 (SUMO-specific proteases 3), a member of the small ubiquitin-like modifier specific protease family, was identified as a molecule that deconjugates SUMOylation of modified protein substrates and functions as an isopeptidase by disrupting SUMO homeostasis to facilitate cancer development and progression. However, its expression and function in nervous system injury and repair are still unclear. In this study, we employed an acute spinal cord injury (SCI) model in adult rats and investigated the dynamic changes of SENP3 expression in the spinal cord. Western blot analysis indicated a gradual increase in SENP3 expression, which peaked 3 days after SCI, and then declined over the following days. Immunohistochemistry results further confirmed that SENP3 was expressed at low levels in the gray and white matter in the non-injured condition and increased after SCI. Moreover, immunofluorescence double-labeling showed that SENP3 was co-expressed with the neuronal marker, NeuN. Furthermore, the SENP3-positive cells that were co-expressed with NeuN had also expressed active caspase-3 after injury. To investigate whether SENP3 plays a role in neuronal apoptosis, we applied H$_{2}$O$_{2}$ to induce neuronal apoptosis in vitro. Western blot analysis showed a significant upregulation of SENP3 and active caspase-3 following H$_{2}$O$_{2}$ stimulation. Taken together, these results suggest that SENP3 may play important roles in the pathophysiology of SCI.
Starting Page	2758
Ending Page	2766
Page Count	9
File Format	PDF
ISSN	03643190
Journal	Neurochemical Research
Volume Number	37
Issue Number	12
e-ISSN	15736903
Language	English
Publisher	Springer US
Publisher Date	2012-09-30
Publisher Place	Boston
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	SCI SENP3 Neuron Apoptosis Neurosciences Neurochemistry Biochemistry Cell Biology Neurology
Content Type	Text
Resource Type	Article
Subject	Medicine Biochemistry 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

The Expression of IGFBP6 after Spinal Cord Injury: Implications for Neuronal Apoptosis

An Up-regulation of IRF-1 After a Spinal Cord Injury: Implications for Neuronal Apoptosis

PCBP2 Modulates Neural Apoptosis and Astrocyte Proliferation After Spinal Cord Injury

The Expression of VHL (Von Hippel-Lindau) After Traumatic Spinal Cord Injury and Its Role in Neuronal Apoptosis

Erratum to: An Up-regulation of IRF-1 After a Spinal Cord Injury: Implications for Neuronal Apoptosis

An Upregulation of SIAH1 After Spinal Cord Injury in Adult Rats

Naringin Treatment Improves Functional Recovery by Increasing BDNF and VEGF Expression, Inhibiting Neuronal Apoptosis After Spinal Cord Injury

PRDM5 Expression and Essential Role After Acute Spinal Cord Injury in Adult Rat

MCM7 Expression Is Altered in Rat After Spinal Cord Injury

An Upregulation of SENP3 After Spinal Cord Injury: Implications for Neuronal Apoptosis

Similar Documents

The Expression of IGFBP6 after Spinal Cord Injury: Implications for Neuronal Apoptosis

An Up-regulation of IRF-1 After a Spinal Cord Injury: Implications for Neuronal Apoptosis

PCBP2 Modulates Neural Apoptosis and Astrocyte Proliferation After Spinal Cord Injury

The Expression of VHL (Von Hippel-Lindau) After Traumatic Spinal Cord Injury and Its Role in Neuronal Apoptosis

Erratum to: An Up-regulation of IRF-1 After a Spinal Cord Injury: Implications for Neuronal Apoptosis

An Upregulation of SIAH1 After Spinal Cord Injury in Adult Rats

Naringin Treatment Improves Functional Recovery by Increasing BDNF and VEGF Expression, Inhibiting Neuronal Apoptosis After Spinal Cord Injury

PRDM5 Expression and Essential Role After Acute Spinal Cord Injury in Adult Rat

MCM7 Expression Is Altered in Rat After Spinal Cord Injury

An Upregulation of SENP3 After Spinal Cord Injury: Implications for Neuronal Apoptosis