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MT5‐MMP controls APP and β‐CTF/C99 metabolism through proteolytic‐dependent and ‐independent mechanisms relevant for Alzheimer's disease
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Abstract
We previously discovered the implication of membrane‐type 5‐matrix metalloproteinase (MT5‐MMP) in Alzheimer's disease (AD) pathogenesis. Here, we shed new light on pathogenic mechanisms by which MT5‐MMP controls the processing of amyloid precursor protein (APP) and the fate of amyloid beta peptide (Aβ) as well as its precursor C99, and C83. We found in human embryonic kidney cells (HEK) carrying the APP Swedish familial mutation (HEKswe) that deleting the C‐terminal non‐catalytic domains of MT5‐MMP hampered its ability to process APP and release the soluble 95 kDa form (sAPP95). Catalytically inactive MT5‐MMP variants increased the levels of Aβ and promoted APP/C99 sorting in the endolysosomal system, likely through interactions of the proteinase C‐terminal portion with C99. Most interestingly, the deletion of the C‐terminal domain of MT5‐MMP caused a strong degradation of C99 by the proteasome and prevented Aβ accumulation. These discoveries reveal new control of MT5‐MMP over APP by proteolytic and non‐proteolytic mechanisms driven by the C‐terminal domains of the proteinase. The targeting of these non‐catalytic domains of MT5‐MMP could, therefore, provide new insights into the therapeutic regulation of APP‐related pathology in AD.
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For each experiment, cDNA samples were analyzed in duplicate and relative gene expression was obtained using the comparative 2−(ΔΔCt) method after normalization to the Gapdh housekeeping gene.
“For each experiment, cDNA samples were analyzed in duplicate and relative gene expression was obtained using the comparative 2−(ΔΔCt) method after normalization to the Gapdh (Mm99999915_g1) housekeeping gene [32, 33].”
C83 is a preferential substrate of γ-secretase and the most abundant APP fragment in cultured neurons.
“consistent with C83 being a preferential substrate of γ-secretase [32] and the most abundant APP fragment in cultured neurons [15, 16]”
MT5-MMP deficiency facilitates C99 degradation in these neurons.
“MT5-MMP deficiency facilitates C99 degradation in these neurons, which supports our recent results in HEK cells showing that deletion of C-terminal domains of MT5-MMP does indeed lead to C99 degradation [32].”
Non-catalytic interactions of MT5-MMP promote C99 degradation by the proteasome and, to a lesser extent, by lysosomes.
“non-catalytic interactions of MT5-MMP promote C99 degradation by the proteasome and, to a lesser extent, by lysosomes [32].”
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Cites
Not just amyloid: physiological functions of the amyloid precursor protein family
Müller, U. C., Deller, T., & Korte, M. (2017) · Nature Reviews Neuroscience · doi:10.1038/nrn.2017.29 · Cited by 634
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η-Secretase processing of APP inhibits neuronal activity in the hippocampus
Willem, M., Tahirovic, S., Busche, M. A., Ovsepian, S. V., Chafai, M., Kootar, S., Hornburg, D., Evans, L. D. B., Moore, S., Daria, A., et al. (2015) · Nature · doi:10.1038/nature14864 · Cited by 398
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Self-citationMatrix Metalloproteinases as New Targets in Alzheimer’s Disease: Opportunities and Challenges
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Pilat, D., Paumier, J.-M., García-González, L., Louis, L., Stephan, D., Manrique, C., Khrestchatisky, M., Di Pasquale, E., Baranger, K., & Rivera, S. (2022) · Journal of Neuroinflammation · doi:10.1186/s12974-022-02407-z · Cited by 28
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Metadata
- Authors
- García‐González, L., Paumier, J., Louis, L., Pilat, D., Bernard, A., Stephan, D., Jullien, N., Checler, F., Nivet, E., Khrestchatisky, M., Baranger, K., & Rivera, S.
- Affiliations
- Aix‐Marseille Univ CNRS, INP, Inst Neurophysiopathol Marseille France
- IPMC UMR 7275 CNRS‐UCA Labex DistAlz Valbonne France
- ORCID
- Rivera, Santiago
- Venue
- The FASEB Journal
- Publisher
- Wiley
- Published
- 2021-06-12
- Volume
- 35
- Issue
- 7
- ISSN
- 0892-6638
- 1530-6860
- Cited by
- 16
- References
- 7
- Language
- en
- Licence
- Funders
- Centre National de la Recherche Scientifique
- Aix-Marseille Université
- Agence Nationale de la Recherche
- Fondation Plan Alzheimer
- Association France Alzheimer
- Fondation pour la Recherche Médicale (FDT201904008423, FDT202001011017)
- Labex
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