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Cited by 234Immune Response and InflammationNeuroinflammation and Neurodegeneration MechanismsCell death mechanisms and regulation

MyD88-5 links mitochondria, microtubules, and JNK3 in neurons and regulates neuronal survival

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Kim, Younghwa, Zhou, Ping, Qian, Liping, Chuang, Jen-Zen, Lee, Jessica, Li, Chenjian, Iadecola, Costantino, Nathan, Carl, Ding, Aihao·2007·The Journal of Experimental Medicine
DOI 10.1084/jem.20070868PMC PMC2118693
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Abstract

The innate immune system relies on evolutionally conserved Toll-like receptors (TLRs) to recognize diverse microbial molecular structures. Most TLRs depend on a family of adaptor proteins termed MyD88s to transduce their signals. Critical roles of MyD88-1–4 in host defense were demonstrated by defective immune responses in knockout mice. In contrast, the sites of expression and functions of vertebrate MyD88-5 have remained elusive. We show that MyD88-5 is distinct from other MyD88s in that MyD88-5 is preferentially expressed in neurons, colocalizes in part with mitochondria and JNK3, and regulates neuronal death. We prepared MyD88-5/GFP transgenic mice via a bacterial artificial chromosome to preserve its endogenous expression pattern. MyD88-5/GFP was detected chiefly in the brain, where it associated with punctate structures within neurons and copurified in part with mitochondria. In vitro, MyD88-5 coimmunoprecipitated with JNK3 and recruited JNK3 from cytosol to mitochondria. Hippocampal neurons from MyD88-5–deficient mice were protected from death after deprivation of oxygen and glucose. In contrast, MyD88-5–null macrophages behaved like wild-type cells in their response to microbial products. Thus, MyD88-5 appears unique among MyD88s in functioning to mediate stress-induced neuronal toxicity.

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Cited by

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Authors
Kim, Y., Zhou, P., Qian, L., Chuang, J.-Z., Lee, J., Li, C., Iadecola, C., Nathan, C., & Ding, A.
Affiliations
  • Cornell University (US)
  • 2Division of Neurobiology, Department of Neurology and Neuroscience,
  • 1Department of Microbiology and Immunology
ORCID
Venue
The Journal of Experimental Medicine
Publisher
Rockefeller University Press
Published
2007-08-27
Volume
204
Issue
9
Pages
2063-2074
ISSN
  • 0022-1007 (ISSN-L)
  • 1540-9538
DOI
10.1084/jem.20070868
PMC
PMC2118693
OpenAlex
W2109130014
Cited by
234
References
3
Citations by year
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FWCI
3.72
Type
journal article
Language
en
Open access
Licence
cc-by-nc-sa
Locations
  • The Journal of Experimental Medicine (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-sa)
  • PubMed Central (publishedVersion, cc-by-nc-sa)
  • PubMed (publishedVersion)
Funders
  • National Institute of General Medical Sciences (R01GM061710, GM61710)
  • National Institute of Allergy and Infectious Diseases (AI 30165, R01AI030165)
  • National Institute of Neurological Disorders and Stroke (R01NS034179, R01NS035806, NS34179, NS-35806, R37NS034179)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
Keywords
Toll-like receptors, JNK3, mitochondria, microtubules, neuronal survival, neuronal cell death, oxygen-glucose deprivation, hippocampal neurons, macrophages, innate immunity
MeSH terms
Animals, Cell Compartmentation, Cell Survival, Glucose, Hippocampus, Mice, Inbred C57BL, Microtubules, Mitochondria, Neurons, Oxygen, Protein Binding, Cell Death, Conserved Sequence, Mice, Knockout, Evolution, Molecular, Protein Transport, Myeloid Cells, Mitogen-Activated Protein Kinase 10, Mice, Myeloid Differentiation Factor 88

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