PACAP and VIP Mitigate Rotenone-Induced Inflammation in BV-2 Microglial Cells.

Broome, ST; Musumeci, G; Castorina, A

PACAP and VIP Mitigate Rotenone-Induced Inflammation in BV-2 Microglial Cells.

Broome, ST Musumeci, G Castorina, A

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Publisher:: Springer Science and Business Media LLC
Publication Type:: Journal Article
Citation:: J Mol Neurosci, 2022, pp. 1-13
Issue Date:: 2022-02-24

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Field	Value	Language
dc.contributor.author	Broome, ST
dc.contributor.author	Musumeci, G
dc.contributor.author	Castorina, A https://orcid.org/0000-0001-7037-759X
dc.date.accessioned	2022-03-08T06:27:51Z
dc.date.available	2022-01-05
dc.date.available	2022-03-08T06:27:51Z
dc.date.issued	2022-02-24
dc.identifier.citation	J Mol Neurosci, 2022, pp. 1-13
dc.identifier.issn	0895-8696
dc.identifier.issn	1559-1166
dc.identifier.uri	http://hdl.handle.net/10453/155075
dc.description.abstract	Rotenone is a commercial pesticide commonly used to model Parkinson's disease (PD) due to its ability to induce dopaminergic degeneration. Studies have confirmed that rotenone causes microglial activation, which seems to contribute to the toxic effects seen in rodent models. Pituitary adenylate cyclase-activating polypeptide (PACAP) and vasoactive intestinal peptide (VIP) are two structurally related neuropeptides that have robust neuroprotective and anti-inflammatory properties. However, their ability to regulate microglial activity in response to rotenone is not fully understood. Using rotenone as an inflammatory stimulus, we tested whether PACAP or VIP could mitigate microglial activation in BV2 microglial cells. Rotenone dose-dependently reduced cell viability and the percentage of apoptotic cells. It also increased the release of nitric oxide (NO) in culture media and the expression of microglial activation markers and pro-inflammatory markers, including CD11b, MMP-9 and IL-6, and heightened the endogenous levels of PACAP and its preferring receptor PAC1. Co-treatment with PACAP or VIP prevented rotenone-induced increase of NO, CD11b, MMP-9 and IL-6. These results indicate that both PACAP and VIP are able to prevent the pro-inflammatory effects of rotenone in BV2 cells, supporting the idea that these molecules can have therapeutic value in slowing down PD progression.
dc.format	Print-Electronic
dc.language	eng
dc.publisher	Springer Science and Business Media LLC
dc.relation.ispartof	J Mol Neurosci
dc.relation.isbasedon	10.1007/s12031-022-01968-1
dc.rights	info:eu-repo/semantics/openAccess
dc.subject	1109 Neurosciences, 1702 Cognitive Sciences
dc.subject.classification	Neurology & Neurosurgery
dc.title	PACAP and VIP Mitigate Rotenone-Induced Inflammation in BV-2 Microglial Cells.
dc.type	Journal Article
utslib.location.activity	United States
utslib.for	1109 Neurosciences
utslib.for	1702 Cognitive Sciences
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	2022-03-08T06:27:42Z
pubs.publication-status	Published online

Abstract:

Rotenone is a commercial pesticide commonly used to model Parkinson's disease (PD) due to its ability to induce dopaminergic degeneration. Studies have confirmed that rotenone causes microglial activation, which seems to contribute to the toxic effects seen in rodent models. Pituitary adenylate cyclase-activating polypeptide (PACAP) and vasoactive intestinal peptide (VIP) are two structurally related neuropeptides that have robust neuroprotective and anti-inflammatory properties. However, their ability to regulate microglial activity in response to rotenone is not fully understood. Using rotenone as an inflammatory stimulus, we tested whether PACAP or VIP could mitigate microglial activation in BV2 microglial cells. Rotenone dose-dependently reduced cell viability and the percentage of apoptotic cells. It also increased the release of nitric oxide (NO) in culture media and the expression of microglial activation markers and pro-inflammatory markers, including CD11b, MMP-9 and IL-6, and heightened the endogenous levels of PACAP and its preferring receptor PAC1. Co-treatment with PACAP or VIP prevented rotenone-induced increase of NO, CD11b, MMP-9 and IL-6. These results indicate that both PACAP and VIP are able to prevent the pro-inflammatory effects of rotenone in BV2 cells, supporting the idea that these molecules can have therapeutic value in slowing down PD progression.

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http://hdl.handle.net/10453/155075