Potential Crosstalk between the PACAP/VIP Neuropeptide System and Endoplasmic Reticulum Stress-Relevance to Multiple Sclerosis Pathophysiology.

Withana, M; Castorina, A

Potential Crosstalk between the PACAP/VIP Neuropeptide System and Endoplasmic Reticulum Stress-Relevance to Multiple Sclerosis Pathophysiology.

Withana, M Castorina, A

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Publisher:: MDPI
Publication Type:: Journal Article
Citation:: Cells, 2023, 12, (22), pp. 2633
Issue Date:: 2023-11-15

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Field	Value	Language
dc.contributor.author	Withana, M
dc.contributor.author	Castorina, A https://orcid.org/0000-0001-7037-759X
dc.date.accessioned	2024-01-08T05:17:55Z
dc.date.available	2023-11-14
dc.date.available	2024-01-08T05:17:55Z
dc.date.issued	2023-11-15
dc.identifier.citation	Cells, 2023, 12, (22), pp. 2633
dc.identifier.issn	2073-4409
dc.identifier.issn	2073-4409
dc.identifier.uri	http://hdl.handle.net/10453/174095
dc.description.abstract	Multiple sclerosis (MS) is an immune-mediated disorder characterized by focal demyelination and chronic inflammation of the central nervous system (CNS). Although the exact etiology is unclear, mounting evidence indicates that endoplasmic reticulum (ER) stress represents a key event in disease pathogenesis. Pituitary adenylate cyclase-activating peptide (PACAP) and vasoactive intestinal peptide (VIP) are two structurally related neuropeptides that are abundant in the CNS and are known to exert neuroprotective and immune modulatory roles. Activation of this endogenous neuropeptide system may interfere with ER stress processes to promote glial cell survival and myelin self-repair. However, the potential crosstalk between the PACAP/VIP system and ER stress remains elusive. In this review, we aim to discuss how these peptides ameliorate ER stress in the CNS, with a focus on MS pathology. Our goal is to emphasize the importance of this potential interaction to aid in the identification of novel therapeutic targets for the treatment of MS and other demyelinating disorders.
dc.format	Electronic
dc.language	eng
dc.publisher	MDPI
dc.relation.ispartof	Cells
dc.relation.isbasedon	10.3390/cells12222633
dc.rights	info:eu-repo/semantics/openAccess
dc.subject.classification	31 Biological sciences
dc.subject.classification	32 Biomedical and clinical sciences
dc.subject.mesh	Humans
dc.subject.mesh	Vasoactive Intestinal Peptide
dc.subject.mesh	Pituitary Adenylate Cyclase-Activating Polypeptide
dc.subject.mesh	Multiple Sclerosis
dc.subject.mesh	Receptors, Vasoactive Intestinal Peptide
dc.subject.mesh	Receptors, Pituitary Adenylate Cyclase-Activating Polypeptide
dc.subject.mesh	Signal Transduction
dc.subject.mesh	Endoplasmic Reticulum Stress
dc.subject.mesh	Humans
dc.subject.mesh	Multiple Sclerosis
dc.subject.mesh	Vasoactive Intestinal Peptide
dc.subject.mesh	Receptors, Vasoactive Intestinal Peptide
dc.subject.mesh	Signal Transduction
dc.subject.mesh	Pituitary Adenylate Cyclase-Activating Polypeptide
dc.subject.mesh	Receptors, Pituitary Adenylate Cyclase-Activating Polypeptide
dc.subject.mesh	Endoplasmic Reticulum Stress
dc.title	Potential Crosstalk between the PACAP/VIP Neuropeptide System and Endoplasmic Reticulum Stress-Relevance to Multiple Sclerosis Pathophysiology.
dc.type	Journal Article
utslib.citation.volume	12
utslib.location.activity	Switzerland
pubs.organisational-group	/University of Technology Sydney
pubs.organisational-group	/University of Technology Sydney/Faculty of Science
pubs.organisational-group	/University of Technology Sydney/Faculty of Science/School of Life Sciences
pubs.organisational-group	/University of Technology Sydney/Centre for Health Technologies (CHT)
utslib.copyright.status	open_access	*
dc.date.updated	2024-01-08T05:17:53Z
pubs.issue	22
pubs.publication-status	Published online
pubs.volume	12
utslib.citation.issue	22

Abstract:

Multiple sclerosis (MS) is an immune-mediated disorder characterized by focal demyelination and chronic inflammation of the central nervous system (CNS). Although the exact etiology is unclear, mounting evidence indicates that endoplasmic reticulum (ER) stress represents a key event in disease pathogenesis. Pituitary adenylate cyclase-activating peptide (PACAP) and vasoactive intestinal peptide (VIP) are two structurally related neuropeptides that are abundant in the CNS and are known to exert neuroprotective and immune modulatory roles. Activation of this endogenous neuropeptide system may interfere with ER stress processes to promote glial cell survival and myelin self-repair. However, the potential crosstalk between the PACAP/VIP system and ER stress remains elusive. In this review, we aim to discuss how these peptides ameliorate ER stress in the CNS, with a focus on MS pathology. Our goal is to emphasize the importance of this potential interaction to aid in the identification of novel therapeutic targets for the treatment of MS and other demyelinating disorders.

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http://hdl.handle.net/10453/174095