Evidence map›Paper›PMID 26802986›Full record

ArticleBrain, behavior, and immunity2016

MHCI promotes developmental synapse elimination and aging-related synapse loss at the vertebrate neuromuscular junction.

Mazell M Tetruashvily, Marin A McDonald, Karla K Frietze, Lisa M Boulanger

Abstract read
In one paragraph

Article in Brain, behavior, and immunity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

17 citing papers in PubMed.

  1. Review
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  15. EMBO molecular medicine · 2017
    Article
  16. Neuromuscular NMDA Receptors Modulate Developmental Synapse Elimination.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  17. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

Mazell M TetruashvilyDepartment of Molecular Biology, Princeton University, Princeton, NJ 08544, United States; Rutgers Robert Wood Johnson Medical School, Piscataway, NJ 08854, United States.
Marin A McDonaldDepartment of Neurosciences, University of California, San Diego 92093, United States; Medical Scientist Training Program, University of California, San Diego 92093, United States.
Karla K FrietzeDepartment of Molecular Biology, Princeton University, Princeton, NJ 08544, United States.
Lisa M BoulangerDepartment of Molecular Biology, Princeton University, Princeton, NJ 08544, United States; Department of Neurosciences, University of California, San Diego 92093, United States; Princeton Neuroscience Institute, Princeton University, Princeton, NJ 08544, United States. Electronic address: lboulang@princeton.edu.

Funding

PREDOCTORAL TRAINING PROGRAM IN GENETICST32GM007388 · NIGMS · PRINCETON UNIVERSITY · PI CRISTEA, ILEANA M. · 1985 to 2022
$27.4M
MHCI Molecules in Age-Related Synapse Loss at the Neuromuscular JunctionF30AG046044 · NIA · RBHS-ROBERT WOOD JOHNSON MEDICAL SCHOOL · PI TETRUASHVILY, MAZELL M · 2014 to 2018
$243k
NIA NIH HHS F30 AG046044NIGMS NIH HHS T32 GM007388
6 · The paper itself

Abstract

Synapse elimination at the developing neuromuscular junction (NMJ) sculpts motor circuits, and synapse loss at the aging NMJ drives motor impairments that are a major cause of loss of independence in the elderly. Here we provide evidence that at the NMJ, both developmental synapse elimination and aging-related synapse loss are promoted by specific immune proteins, members of the major histocompatibility complex class I (MHCI). MHCI is expressed at the developing NMJ, and three different methods of reducing MHCI function all disrupt synapse elimination during the second postnatal week, leaving some muscle fibers multiply-innervated, despite otherwise outwardly normal synapse formation and maturation. Conversely, overexpressing MHCI modestly accelerates developmental synapse elimination. MHCI levels at the NMJ rise with aging, and reducing MHCI levels ameliorates muscle denervation in aged mice. These findings identify an unexpected role for MHCI in the elimination of neuromuscular synapses during development, and indicate that reducing MHCI levels can preserve youthful innervation of aging muscle.

Indexed as

AgingAnimalsAnimals, NewbornGenes, MHC Class IMiceNeuromuscular JunctionSynapsesAgingDenervationDevelopmentMajor histocompatibility complex class IMHCINeuromuscular junctionNMJSynapse elimination

Identifiers

PMID26802986
PMCPMC5813483

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.