A new role for matrix metalloproteinase-3 in the NGF metabolic pathway: Proteolysis of mature NGF and sex-specific differences in the continuum of Alzheimer's pathology.


Journal

Neurobiology of disease
ISSN: 1095-953X
Titre abrégé: Neurobiol Dis
Pays: United States
ID NLM: 9500169

Informations de publication

Date de publication:
01 2021
Historique:
received: 09 08 2020
revised: 20 10 2020
accepted: 23 10 2020
pubmed: 2 11 2020
medline: 15 12 2021
entrez: 1 11 2020
Statut: ppublish

Résumé

Matrix metalloproteinase-3 (MMP-3) has been associated with risk of Alzheimer's disease (AD). In this study we introduce a novel role for MMP-3 in degrading nerve growth factor (NGF) in vivo and examine its mRNA and protein expression across the continuum of AD pathology. We provide evidence that MMP-3 participates in the degradation of mature NGF in vitro and in vivo and that it is secreted from the rat cerebral cortex in an activity-dependent manner. We show that cortical MMP-3 is upregulated in the McGill-R-Thy1-APP transgenic rat model of AD-like amyloidosis. A similar upregulation was found in AD and MCI brains as well as in cognitively normal individuals with elevated amyloid deposition. We also observed that frontal cortex MMP-3 protein levels are higher in males. MMP-3 protein correlated with more AD neuropathology, markers of NGF metabolism, and lower cognitive scores in males but not in females. These results suggest that MMP-3 upregulation in AD might contribute to NGF dysmetabolism, and therefore to cholinergic atrophy and cognitive deficits, in a sex-specific manner. MMP-3 should be further investigated as a biomarker candidate or as a therapeutic target in AD.

Identifiants

pubmed: 33130223
pii: S0969-9961(20)30425-3
doi: 10.1016/j.nbd.2020.105150
pmc: PMC7856186
mid: NIHMS1650339
pii:
doi:

Substances chimiques

RNA, Messenger 0
Nerve Growth Factor 9061-61-4
Matrix Metalloproteinase 3 EC 3.4.24.17

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

105150

Subventions

Organisme : NIA NIH HHS
ID : P30 AG010161
Pays : United States
Organisme : NIA NIH HHS
ID : R01 AG015819
Pays : United States
Organisme : NIA NIH HHS
ID : RF1 AG056850
Pays : United States
Organisme : CIHR
ID : 20129MOP-285643-PT-CFAA-22808
Pays : Canada

Informations de copyright

Copyright © 2020 The Authors. Published by Elsevier Inc. All rights reserved.

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Auteurs

Rowan Pentz (R)

Department of Neurology and Neurosurgery, McGill University, Montreal, Canada. Electronic address: rowan.pentz@mail.mcgill.ca.

M Florencia Iulita (MF)

Department of Pharmacology and Therapeutics, McGill University, Montreal, Canada; Sant Pau Memory Unit, Department of Neurology, Hospital de la Santa Creu i Sant Pau, Biomedical Research Institute Sant Pau, Universitat Autònoma de Barcelona, Barcelona, Spain. Electronic address: florencia.iulita@gmail.com.

Maya Mikutra-Cencora (M)

Department of Pharmacology and Therapeutics, McGill University, Montreal, Canada. Electronic address: maya.mikutra-cencora@umontreal.ca.

Adriana Ducatenzeiler (A)

Department of Pharmacology and Therapeutics, McGill University, Montreal, Canada. Electronic address: Adriana.ducatenzeiler@mcgill.ca.

David A Bennett (DA)

Rush Alzheimer's Disease Center, Rush University Medical Center, Chicago, IL, USA. Electronic address: David_A_Bennett@rush.edu.

A Claudio Cuello (AC)

Department of Neurology and Neurosurgery, McGill University, Montreal, Canada; Department of Pharmacology and Therapeutics, McGill University, Montreal, Canada; Department of Anatomy and Cell Biology, McGill University, Montreal, Canada. Electronic address: claudio.cuello@mcgill.ca.

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Classifications MeSH