TREM2 interacts with TDP-43 and mediates microglial neuroprotection against TDP-43-related neurodegeneration.


Journal

Nature neuroscience
ISSN: 1546-1726
Titre abrégé: Nat Neurosci
Pays: United States
ID NLM: 9809671

Informations de publication

Date de publication:
01 2022
Historique:
received: 21 12 2020
accepted: 02 11 2021
pubmed: 18 12 2021
medline: 7 4 2022
entrez: 17 12 2021
Statut: ppublish

Résumé

Triggering receptor expressed on myeloid cell 2 (TREM2) is linked to risk of neurodegenerative disease. However, the function of TREM2 in neurodegeneration is still not fully understood. Here, we investigated the role of microglial TREM2 in TAR DNA-binding protein 43 (TDP-43)-related neurodegeneration using virus-mediated and transgenic mouse models. We found that TREM2 deficiency impaired phagocytic clearance of pathological TDP-43 by microglia and enhanced neuronal damage and motor impairments. Mass cytometry analysis revealed that human TDP-43 (hTDP-43) induced a TREM2-dependent subpopulation of microglia with high CD11c expression and phagocytic ability. Using mass spectrometry (MS) and surface plasmon resonance (SPR) analysis, we further demonstrated an interaction between TDP-43 and TREM2 in vitro and in vivo as well as in human tissues from individuals with amyotrophic lateral sclerosis (ALS). We computationally identified regions within hTDP-43 that interact with TREM2. Our data highlight that TDP-43 is a possible ligand for microglial TREM2 and that this interaction mediates neuroprotection of microglia in TDP-43-related neurodegeneration.

Identifiants

pubmed: 34916658
doi: 10.1038/s41593-021-00975-6
pii: 10.1038/s41593-021-00975-6
pmc: PMC8741737
mid: NIHMS1753734
doi:

Substances chimiques

DNA-Binding Proteins 0
Membrane Glycoproteins 0
Receptors, Immunologic 0
TDP-43 protein, mouse 0
Trem2 protein, mouse 0

Types de publication

Journal Article Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

26-38

Subventions

Organisme : NINDS NIH HHS
ID : R01 NS110949
Pays : United States
Organisme : NIA NIH HHS
ID : U19 AG069701
Pays : United States
Organisme : NIA NIH HHS
ID : R01 AG066395
Pays : United States
Organisme : NIA NIH HHS
ID : R21 AG064159
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS088627
Pays : United States

Informations de copyright

© 2022. The Author(s), under exclusive licence to Springer Nature America, Inc.

Références

Hickman, S., Izzy, S., Sen, P., Morsett, L. & El Khoury, J. Microglia in neurodegeneration. Nat. Neurosci. 21, 1359–1369 (2018).
pubmed: 30258234 pmcid: 6817969 doi: 10.1038/s41593-018-0242-x
Ulland, T. K. & Colonna, M. TREM2—a key player in microglial biology and Alzheimer disease. Nat. Rev. Neurol. 14, 667–675 (2018).
pubmed: 30266932 doi: 10.1038/s41582-018-0072-1
Guerreiro, R. et al. TREM2 variants in Alzheimer’s disease. N. Engl. J. Med. 368, 117–127 (2013).
pubmed: 23150934 doi: 10.1056/NEJMoa1211851
Jonsson, T. et al. Variant of TREM2 associated with the risk of Alzheimer’s disease. N. Engl. J. Med. 368, 107–116 (2013).
pubmed: 23150908 doi: 10.1056/NEJMoa1211103
Wang, Y. et al. TREM2 lipid sensing sustains the microglial response in an Alzheimer’s disease model. Cell 160, 1061–1071 (2015).
pubmed: 25728668 pmcid: 4477963 doi: 10.1016/j.cell.2015.01.049
Zhao, Y. et al. TREM2 is a receptor for β-amyloid that mediates microglial function. Neuron 97, 1023–1031 (2018).
pubmed: 29518356 pmcid: 5889092 doi: 10.1016/j.neuron.2018.01.031
Ou, S. H., Wu, F., Harrich, D., Garcia-Martinez, L. F. & Gaynor, R. B. Cloning and characterization of a novel cellular protein, TDP-43, that binds to human immunodeficiency virus type 1 TAR DNA sequence motifs. J. Virol. 69, 3584–3596 (1995).
pubmed: 7745706 pmcid: 189073 doi: 10.1128/jvi.69.6.3584-3596.1995
Neumann, M. et al. Ubiquitinated TDP-43 in frontotemporal lobar degeneration and amyotrophic lateral sclerosis. Science 314, 130–133 (2006).
pubmed: 17023659 doi: 10.1126/science.1134108
Cairns, N. J. et al. TDP-43 in familial and sporadic frontotemporal lobar degeneration with ubiquitin inclusions. Am. J. Pathol. 171, 227–240 (2007).
pubmed: 17591968 pmcid: 1941578 doi: 10.2353/ajpath.2007.070182
Cady, J. et al. TREM2 variant p.R47H as a risk factor for sporadic amyotrophic lateral sclerosis. JAMA Neurol. 71, 449–453 (2014).
pubmed: 24535663 pmcid: 4087113 doi: 10.1001/jamaneurol.2013.6237
Rayaprolu, S. et al. TREM2 in neurodegeneration: evidence for association of the p.R47H variant with frontotemporal dementia and Parkinson’s disease. Mol. Neurodegener. 8, 19 (2013).
pubmed: 23800361 pmcid: 3691612 doi: 10.1186/1750-1326-8-19
Krasemann, S. et al. The TREM2–APOE pathway drives the transcriptional phenotype of dysfunctional microglia in neurodegenerative diseases. Immunity 47, 566–581 (2017).
pubmed: 28930663 pmcid: 5719893 doi: 10.1016/j.immuni.2017.08.008
Maniatis, S. et al. Spatiotemporal dynamics of molecular pathology in amyotrophic lateral sclerosis. Science 364, 89–93 (2019).
pubmed: 30948552 doi: 10.1126/science.aav9776
Walker, A. K. et al. Functional recovery in new mouse models of ALS/FTLD after clearance of pathological cytoplasmic TDP-43. Acta Neuropathol. 130, 643–660 (2015).
pubmed: 26197969 pmcid: 5127391 doi: 10.1007/s00401-015-1460-x
Perry, V. H., Nicoll, J. A. & Holmes, C. Microglia in neurodegenerative disease. Nat. Rev. Neurol. 6, 193–201 (2010).
pubmed: 20234358 doi: 10.1038/nrneurol.2010.17
Mrdjen, D. et al. High-dimensional single-cell mapping of central nervous system immune cells reveals distinct myeloid subsets in health, aging, and disease. Immunity 48, 380–395 (2018).
pubmed: 29426702 doi: 10.1016/j.immuni.2018.01.011
Keren-Shaul, H. et al. A unique microglia type associated with restricting development of Alzheimer’s disease. Cell 169, 1276–1290 (2017).
pubmed: 28602351 doi: 10.1016/j.cell.2017.05.018
Eyo, U. B. et al. P2Y12R-dependent translocation mechanisms gate the changing microglial landscape. Cell Rep. 23, 959–966 (2018).
pubmed: 29694903 pmcid: 5965271 doi: 10.1016/j.celrep.2018.04.001
Spiller, K. J. et al. Microglia-mediated recovery from ALS-relevant motor neuron degeneration in a mouse model of TDP-43 proteinopathy. Nat. Neurosci. 21, 329–340 (2018).
pubmed: 29463850 pmcid: 5857237 doi: 10.1038/s41593-018-0083-7
Steinacker, P. et al. TDP-43 in cerebrospinal fluid of patients with frontotemporal lobar degeneration and amyotrophic lateral sclerosis. Arch. Neurol. 65, 1481–1487 (2008).
pubmed: 19001167 pmcid: 2690860 doi: 10.1001/archneur.65.11.1481
Zhong, J. et al. The interactome of a PTB domain-containing adapter protein, Odin, revealed by SILAC. J. Proteom. 74, 294–303 (2011).
doi: 10.1016/j.jprot.2010.11.006
Guenther, E. L. et al. Atomic structures of TDP-43 LCD segments and insights into reversible or pathogenic aggregation. Nat. Struct. Mol. Biol. 25, 463–471 (2018).
pubmed: 29786080 pmcid: 5990464 doi: 10.1038/s41594-018-0064-2
Lee, E. B., Lee, V. M. & Trojanowski, J. Q. Gains or losses: molecular mechanisms of TDP43-mediated neurodegeneration. Nat. Rev. Neurosci. 13, 38–50 (2011).
pubmed: 22127299 pmcid: 3285250 doi: 10.1038/nrn3121
Li, Q. et al. Developmental heterogeneity of microglia and brain myeloid cells revealed by deep single-cell RNA sequencing. Neuron 101, 207–223 (2019).
pubmed: 30606613 doi: 10.1016/j.neuron.2018.12.006
Liu, Y. U. et al. Neuronal network activity controls microglial process surveillance in awake mice via norepinephrine signaling. Nat. Neurosci. 22, 1771–1781 (2019).
pubmed: 31636449 pmcid: 6858573 doi: 10.1038/s41593-019-0511-3
Parhizkar, S. et al. Loss of TREM2 function increases amyloid seeding but reduces plaque-associated ApoE. Nat. Neurosci. 22, 191–204 (2019).
pubmed: 30617257 pmcid: 6417433 doi: 10.1038/s41593-018-0296-9
Leyns, C. E. G. et al. TREM2 function impedes tau seeding in neuritic plaques. Nat. Neurosci. 22, 1217–1222 (2019).
pubmed: 31235932 pmcid: 6660358 doi: 10.1038/s41593-019-0433-0
Lee, C. Y. D. et al. Elevated TREM2 gene dosage reprograms microglia responsivity and ameliorates pathological phenotypes in Alzheimer’s disease models. Neuron 97, 1032–1048 (2018).
pubmed: 29518357 pmcid: 5927822 doi: 10.1016/j.neuron.2018.02.002
Konishi, H. & Kiyama, H. Microglial TREM2/DAP12 signaling: a double-edged sword in neural diseases. Front. Cell. Neurosci. 12, 206 (2018).
pubmed: 30127720 pmcid: 6087757 doi: 10.3389/fncel.2018.00206
Mazaheri, F. et al. TREM2 deficiency impairs chemotaxis and microglial responses to neuronal injury. EMBO Rep. 18, 1186–1198 (2017).
pubmed: 28483841 pmcid: 5494532 doi: 10.15252/embr.201743922
Zheng, H. et al. TREM2 promotes microglial survival by activating Wnt/β-catenin pathway. J. Neurosci. 37, 1772–1784 (2017).
pubmed: 28077724 pmcid: 5320608 doi: 10.1523/JNEUROSCI.2459-16.2017
Guan, Z. et al. Injured sensory neuron-derived CSF1 induces microglial proliferation and DAP12-dependent pain. Nat. Neurosci. 19, 94–101 (2016).
pubmed: 26642091 doi: 10.1038/nn.4189
Gu, N. et al. Spinal microgliosis due to resident microglial proliferation is required for pain hypersensitivity after peripheral nerve injury. Cell Rep. 16, 605–614 (2016).
pubmed: 27373153 pmcid: 4956495 doi: 10.1016/j.celrep.2016.06.018
Otero, K. et al. Macrophage colony-stimulating factor induces the proliferation and survival of macrophages via a pathway involving DAP12 and β-catenin. Nat. Immunol. 10, 734–743 (2009).
pubmed: 19503107 pmcid: 4004764 doi: 10.1038/ni.1744
Brown, G. C. & Neher, J. J. Microglial phagocytosis of live neurons. Nat. Rev. Neurosci. 15, 209–216 (2014).
pubmed: 24646669 doi: 10.1038/nrn3710
Fu, R., Shen, Q., Xu, P., Luo, J. J. & Tang, Y. Phagocytosis of microglia in the central nervous system diseases. Mol. Neurobiol. 49, 1422–1434 (2014).
pubmed: 24395130 pmcid: 4012154 doi: 10.1007/s12035-013-8620-6
Hong, S. et al. Complement and microglia mediate early synapse loss in Alzheimer mouse models. Science 352, 712–716 (2016).
pubmed: 27033548 pmcid: 5094372 doi: 10.1126/science.aad8373
Koizumi, S. et al. UDP acting at P2Y6 receptors is a mediator of microglial phagocytosis. Nature 446, 1091–1095 (2007).
pubmed: 17410128 pmcid: 3464483 doi: 10.1038/nature05704
Tufail, Y. et al. Phosphatidylserine exposure controls viral innate immune responses by microglia. Neuron 93, 574–586 e578 (2017).
pubmed: 28111081 pmcid: 5600182 doi: 10.1016/j.neuron.2016.12.021
Das, R. & Chinnathambi, S. Microglial priming of antigen presentation and adaptive stimulation in Alzheimer’s disease. Cell. Mol. Life Sci. 76, 3681–3694 (2019).
pubmed: 31093687 doi: 10.1007/s00018-019-03132-2
Harms, A. S. et al. MHCII is required for α-synuclein-induced activation of microglia, CD4 T cell proliferation, and dopaminergic neurodegeneration. J. Neurosci. 33, 9592–9600 (2013).
pubmed: 23739956 pmcid: 3903980 doi: 10.1523/JNEUROSCI.5610-12.2013
Bulloch, K. et al. CD11c/EYFP transgene illuminates a discrete network of dendritic cells within the embryonic, neonatal, adult, and injured mouse brain. J. Comp. Neurol. 508, 687–710 (2008).
pubmed: 18386786 doi: 10.1002/cne.21668
Sheean, R. K. et al. Association of regulatory T-cell expansion with progression of amyotrophic lateral sclerosis: a study of humans and a transgenic mouse model. JAMA Neurol. 75, 681–689 (2018).
pubmed: 29507931 pmcid: 5885208 doi: 10.1001/jamaneurol.2018.0035
Sato-Hashimoto, M. et al. Microglial SIRPα regulates the emergence of CD11c
doi: 10.7554/eLife.42025
Atagi, Y. et al. Apolipoprotein E is a ligand for triggering receptor expressed on myeloid cells 2 (TREM2). J. Biol. Chem. 290, 26043–26050 (2015).
pubmed: 26374899 pmcid: 4646257 doi: 10.1074/jbc.M115.679043
Feiler, M. S. et al. TDP-43 is intercellularly transmitted across axon terminals. J. Cell Biol. 211, 897–911 (2015).
pubmed: 26598621 pmcid: 4657165 doi: 10.1083/jcb.201504057
Zhong, L. et al. Soluble TREM2 ameliorates pathological phenotypes by modulating microglial functions in an Alzheimer’s disease model. Nat. Commun. 10, 1365 (2019).
pubmed: 30911003 pmcid: 6433910 doi: 10.1038/s41467-019-09118-9
Kober, D. L. et al. Neurodegenerative disease mutations in TREM2 reveal a functional surface and distinct loss-of-function mechanisms. eLife 5, e20391 (2016).
pubmed: 27995897 pmcid: 5173322 doi: 10.7554/eLife.20391
Yeh, F. L., Wang, Y., Tom, I., Gonzalez, L. C. & Sheng, M. TREM2 binds to apolipoproteins, including APOE and CLU/APOJ, and thereby facilitates uptake of amyloid-β by microglia. Neuron 91, 328–340 (2016).
pubmed: 27477018 doi: 10.1016/j.neuron.2016.06.015
Ling, J. P., Pletnikova, O., Troncoso, J. C. & Wong, P. C. TDP-43 repression of nonconserved cryptic exons is compromised in ALS-FTD. Science 349, 650–655 (2015).
pubmed: 26250685 pmcid: 4825810 doi: 10.1126/science.aab0983
Clarkson, B. D. S., Patel, M. S., LaFrance-Corey, R. G. & Howe, C. L. Retrograde interferon-γ signaling induces major histocompatibility class I expression in human-induced pluripotent stem cell-derived neurons. Ann. Clin. Transl Neurol. 5, 172–185 (2018).
pubmed: 29468178 doi: 10.1002/acn3.516
Kim, J.Y., Grunke, S.D., Levites, Y., Golde, T.E. & Jankowsky, J.L. Intracerebroventricular viral injection of the neonatal mouse brain for persistent and widespread neuronal transduction. J. Vis. Exp. https://doi.org/10.3791/51863 (2014).
Peng, J. et al. Microglia and monocytes synergistically promote the transition from acute to chronic pain after nerve injury. Nat. Commun. 7, 12029 (2016).
pubmed: 27349690 pmcid: 4931235 doi: 10.1038/ncomms12029
Gittins, R. & Harrison, P. J. Neuronal density, size and shape in the human anterior cingulate cortex: a comparison of Nissl and NeuN staining. Brain Res. Bull. 63, 155–160 (2004).
pubmed: 15130705 doi: 10.1016/j.brainresbull.2004.02.005
Pang, Y. P. FF12MC: a revised AMBER forcefield and new protein simulation protocol. Proteins 84, 1490–1516 (2016).
pubmed: 27348292 pmcid: 5129589 doi: 10.1002/prot.25094
Jorgensen, W. L., Chandreskhar, J., Madura, J. D., Impey, R. W. & Klein, M. L. Comparison of simple potential functions for simulating liquid water. J. Chem. Phys. 79, 926–935 (1983).
doi: 10.1063/1.445869
Pang, Y.-P. Use of 1–4 interaction scaling factors to control the conformational equilibrium between α-helix and β-strand. Biochem. Biophys. Res. Commun. 457, 183–186 (2015).
pubmed: 25543060 doi: 10.1016/j.bbrc.2014.12.084
Larini, L., Mannella, R. & Leporini, D. Langevin stabilization of molecular-dynamics simulations of polymers by means of quasisymplectic algorithms. J. Chem. Phys. 126, 104101 (2007).
pubmed: 17362055 doi: 10.1063/1.2464095
Darden, T. A., York, D. M. & Pedersen, L. G. Particle mesh Ewald: an N log(N) method for Ewald sums in large systems. J. Chem. Phys. 98, 10089–10092 (1993).
doi: 10.1063/1.464397
Pang, Y. P. Low-mass molecular dynamics simulation for configurational sampling enhancement: more evidence and theoretical explanation. Biochem. Biophys. Rep. 4, 126–133 (2015).
pubmed: 29124195 pmcid: 5668912
Joung, I. S. & Cheatham, T. E. Determination of alkali and halide monovalent ion parameters for use in explicitly solvated biomolecular simulations. J. Phys. Chem. B 112, 9020–9041 (2008).
pubmed: 18593145 pmcid: 2652252 doi: 10.1021/jp8001614
Zhang, J. et al. Neurotoxic microglia promote TDP-43 proteinopathy in progranulin deficiency. Nature 588, 459–465 (2020).
pubmed: 32866962 pmcid: 7746606 doi: 10.1038/s41586-020-2709-7
Perez-Riverol, Y. et al. The PRIDE database and related tools and resources in 2019: improving support for quantification data. Nucleic Acids Res. 47, D442–D450 (2019).
pubmed: 30395289

Auteurs

Manling Xie (M)

Department of Neurology, Mayo Clinic, Rochester, MN, USA.
Mayo Clinic Graduate School of Biomedical Sciences, Rochester, MN, USA.

Yong U Liu (YU)

Department of Neurology, Mayo Clinic, Rochester, MN, USA. liuy6@foxmail.com.
Laboratory for Neuroscience in Health and Disease, Guangzhou First People's Hospital School of Medicine, South China University of Technology, Guangzhou, China. liuy6@foxmail.com.

Shunyi Zhao (S)

Department of Neurology, Mayo Clinic, Rochester, MN, USA.

Lingxin Zhang (L)

Division of Clinical Pharmacology, Department of Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, Rochester, MN, USA.

Dale B Bosco (DB)

Department of Neurology, Mayo Clinic, Rochester, MN, USA.

Yuan-Ping Pang (YP)

Computer-Aided Molecular Design Laboratory, Mayo Clinic, Rochester, MN, USA.

Jun Zhong (J)

Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN, USA.

Udit Sheth (U)

Mayo Clinic Graduate School of Biomedical Sciences, Rochester, MN, USA.
Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA.

Yuka A Martens (YA)

Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA.

Na Zhao (N)

Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA.

Chia-Chen Liu (CC)

Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA.

Yongxian Zhuang (Y)

Division of Clinical Pharmacology, Department of Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, Rochester, MN, USA.

Liewei Wang (L)

Division of Clinical Pharmacology, Department of Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, Rochester, MN, USA.

Dennis W Dickson (DW)

Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA.

Mark P Mattson (MP)

Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD, USA.

Guojun Bu (G)

Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA.

Long-Jun Wu (LJ)

Department of Neurology, Mayo Clinic, Rochester, MN, USA. wu.longjun@mayo.edu.
Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA. wu.longjun@mayo.edu.
Department of Immunology, Mayo Clinic, Rochester, MN, USA. wu.longjun@mayo.edu.

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