NDLI: Autophagy Inhibition Favors Survival of Rubrospinal Neurons After Spinal Cord Hemisection

Content Provider	Springer Nature Link
Author	Bisicchia, Elisa Latini, Laura Cavallucci, Virve Sasso, Valeria Nicolin, Vanessa Molinari, Marco D’Amelio, Marcello Viscomi, Maria Teresa
Copyright Year	2016
Abstract	Spinal cord injuries (SCIs) are devastating conditions of the central nervous system (CNS) for which there are no restorative therapies. Neuronal death at the primary lesion site and in remote regions that are functionally connected to it is one of the major contributors to neurological deficits following SCI.Disruption of autophagic flux induces neuronal death in many CNS injuries, but its mechanism and relationship with remote cell death after SCI are unknown. We examined the function and effects of the modulation of autophagy on the fate of axotomized rubrospinal neurons in a rat model of spinal cord dorsal hemisection (SCH) at the cervical level. Following SCH, we observed an accumulation of LC3-positive autophagosomes (APs) in the axotomized neurons 1 and 5 days after injury. Furthermore, this accumulation was not attributed to greater initiation of autophagy but was caused by a decrease in AP clearance, as demonstrated by the build-up of p62, a widely used marker of the induction of autophagy. In axotomized rubrospinal neurons, the disruption of autophagic flux correlated strongly with remote neuronal death and worse functional recovery. Inhibition of AP biogenesis by 3-methyladenine (3-MA) significantly attenuated remote degeneration and improved spontaneous functional recovery, consistent with the detrimental effects of autophagy in remote damage after SCH. Collectively, our results demonstrate that autophagic flux is blocked in axotomized neurons on SCI and that the inhibition of AP formation improves their survival. Thus, autophagy is a promising target for the development of therapeutic interventions in the treatment of SCIs.
Starting Page	4896
Ending Page	4907
Page Count	12
File Format	PDF
ISSN	08937648
Journal	Molecular Neurobiology
Volume Number	54
Issue Number	7
e-ISSN	15591182
Language	English
Publisher	Springer US
Publisher Date	2016-08-11
Publisher Place	New York
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Autophagy Autophagy flux Spinal cord injury Neurodegeneration Autophagosomes Remote damage 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

Metformin Improves Functional Recovery After Spinal Cord Injury via Autophagy Flux Stimulation

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

Aquaporin-4 Mitigates Retrograde Degeneration of Rubrospinal Neurons by Facilitating Edema Clearance and Glial Scar Formation After Spinal Cord Injury in Mice

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

Exendin-4 Enhances Motor Function Recovery via Promotion of Autophagy and Inhibition of Neuronal Apoptosis After Spinal Cord Injury in Rats

The “Janus-Faced Role” of Autophagy in Neuronal Sickness: Focus on Neurodegeneration

CCL3 contributes to secondary damage after spinal cord injury

Inhibition of Epidermal Growth Factor Receptor Improves Myelination and Attenuates Tissue Damage of Spinal Cord Injury

Lithium Chloride Facilitates Autophagy Following Spinal Cord Injury via ERK-dependent Pathway

Autophagy Inhibition Favors Survival of Rubrospinal Neurons After Spinal Cord Hemisection

Similar Documents

Metformin Improves Functional Recovery After Spinal Cord Injury via Autophagy Flux Stimulation

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

Aquaporin-4 Mitigates Retrograde Degeneration of Rubrospinal Neurons by Facilitating Edema Clearance and Glial Scar Formation After Spinal Cord Injury in Mice

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

Exendin-4 Enhances Motor Function Recovery via Promotion of Autophagy and Inhibition of Neuronal Apoptosis After Spinal Cord Injury in Rats

The “Janus-Faced Role” of Autophagy in Neuronal Sickness: Focus on Neurodegeneration

CCL3 contributes to secondary damage after spinal cord injury

Inhibition of Epidermal Growth Factor Receptor Improves Myelination and Attenuates Tissue Damage of Spinal Cord Injury

Lithium Chloride Facilitates Autophagy Following Spinal Cord Injury via ERK-dependent Pathway

Autophagy Inhibition Favors Survival of Rubrospinal Neurons After Spinal Cord Hemisection