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Publication

The active contribution of OPCs to neuroinflammation is mediated by LRP1.

Anthony Fernández-Castañeda | Megan S Chappell | Dorian A Rosen | Scott M Seki | Rebecca M Beiter | David M Johanson | Delaney Liskey | Emily Farber | Suna Onengut-Gumuscu | Christopher C Overall | Jeffrey L Dupree | Alban Gaultier
Acta neuropathologica | 2020

Oligodendrocyte progenitor cells (OPCs) account for about 5% of total brain and spinal cord cells, giving rise to myelinating oligodendrocytes that provide electrical insulation to neurons of the CNS. OPCs have also recently been shown to regulate inflammatory responses and glial scar formation, suggesting functions that extend beyond myelination. Low-density lipoprotein receptor-related protein 1 (LRP1) is a multifaceted phagocytic receptor that is highly expressed in several CNS cell types, including OPCs. Here, we have generated an oligodendroglia-specific knockout of LRP1, which presents with normal myelin development, but is associated with better outcomes in two animal models of demyelination (EAE and cuprizone). At a mechanistic level, LRP1 did not directly affect OPC differentiation into mature oligodendrocytes. Instead, animals lacking LRP1 in OPCs in the demyelinating CNS were characterized by a robust dampening of inflammation. In particular, LRP1-deficient OPCs presented with impaired antigen cross-presentation machinery, suggesting a failure to propagate the inflammatory response and thus promoting faster myelin repair and neuroprotection. Our study places OPCs as major regulators of neuroinflammation in an LRP1-dependent fashion.

Pubmed ID: 31552482

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Associated grants

  • Agency: NIGMS NIH HHS, United States
    Id: T32 GM007267
  • Agency: NINDS NIH HHS, United States
    Id: R01 NS083542
  • Agency: National Multiple Sclerosis Society, International
    Id: PP1978
  • Agency: NINDS NIH HHS, United States
    Id: R21 NS111204
  • Agency: NINDS NIH HHS, United States
    Id: F31 NS103327
  • Agency: NIGMS NIH HHS, United States
    Id: T32 GM008328
  • Agency: NIGMS NIH HHS, United States
    Id: T32 GM007055

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B6;129S4-Olig1tm1(cre)Rth/J (organism)

RRID:IMSR_JAX:011105

Mus musculus with name B6;129S4-Olig1tm1(cre)Rth/J from IMSR.

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STOCK Tg(Mobp-EGFP)IN1Gsat/Mmucd (organism)

RRID:MMRRC_030483-UCD

Mus musculus with name STOCK Tg(Mobp-EGFP)IN1Gsat/Mmucd from MMRRC.

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B6;129S7-Lrp1tm2Her/J (organism)

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Mus musculus with name B6;129S7-Lrp1tm2Her/J from IMSR.

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C57BL/6-Tg(TcraTcrb)1100Mjb/J (organism)

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Mus musculus with name C57BL/6-Tg(TcraTcrb)1100Mjb/J from IMSR.

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B6N.Cg-Tg(Pdgfra-cre/ERT)467Dbe/J (organism)

RRID:IMSR_JAX:018280

Mus musculus with name B6N.Cg-Tg(Pdgfra-cre/ERT)467Dbe/J from IMSR.

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The Stimulating Peripheral Activity to Relieve Conditions (SPARC) effort is the result of National Institutes of Health’s (NIH) drive to map out the neural circuitry responsible for visceral control in higher vertebrates. The SPARC Anatomy Working Group (SAWG) is responsible for the integrity of anatomical knowledge in SPARC

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Department of Neurosciences, School of Medicine

University of California, San Diego

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