Evidence map›Paper›PMID 21483793›Full record

ArticlePloS one2011

A potential role for shed soluble major histocompatibility class I molecules as modulators of neurite outgrowth.

Lorraine R Washburn, Dan Zekzer, Shoshana Eitan, Yuxin Lu, Hoa Dang, Blake Middleton, Christopher J Evans, Jide Tian, Daniel L Kaufman

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.2field-weighted citation impact, top 27% of its field
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

20 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Article
  3. Open MHC Class I Conformers: A Look through the Looking Glass.International journal of molecular sciences · 2021
    Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. CNS-wide Sexually Dimorphic Induction of the Major Histocompatibility Complex 1 Pathway With Aging.The journals of gerontology. Series A, Biological sciences and medical sciences · 2017
    Article
  10. Article
  11. The Major Histocompatibility Complex (MHC) in Schizophrenia: A Review.Journal of clinical & cellular immunology · 2016
    Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. MHCI requires MEF2 transcription factors to negatively regulate synapse density during development and in disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013
    Article
  17. Review
  18. Article
  19. Article
  20. Article
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

9 authors at 1 institution in 1 country.

Lorraine R WashburnDepartment of Molecular and Medical Pharmacology, University of California Los Angeles, Los Angeles, California, United States of America.
Dan Zekzer
Shoshana Eitan
Yuxin Lu
Hoa Dang
Blake Middleton
Christopher J Evans
Jide Tian
Daniel L Kaufman
University of California, Los Angeles · US

Funding

MHCI Inhibition of Neuronal Repair ResponsesR21NS047383 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI KAUFMAN, DANIEL · 2004 to 2005
$390k
Characterizing MHCI's neuroactivityR21NS053847 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI KAUFMAN, DANIEL · 2006 to 2007
$377k
NINDS NIH HHS R21 NS047383NINDS NIH HHS R21NS047383NINDS NIH HHS R21 NS053847NINDS NIH HHS R21NS053847
6 · The paper itself

Abstract

The neurobiological activities of classical major histocompatibility class I (MHCI) molecules are just beginning to be explored. To further examine MHCI's actions during the formation of neuronal connections, we cultured embryonic mouse retina explants a short distance from wildtype thalamic explants, or thalami from transgenic mice (termed "NSE-Db") whose neurons express higher levels of MHCI. While retina neurites extended to form connections with wildtype thalami, we were surprised to find that retina neurite outgrowth was very stunted in regions proximal to NSE-Db thalamic explants, suggesting that a diffusible factor from these thalami inhibited retina neurite outgrowth. It has been long known that MHCI-expressing cells release soluble forms of MHCI (sMHCI) due to the shedding of intact MHCI molecules, as well as the alternative exon splicing of its heavy chain or the action proteases which cleave off it's transmembrane anchor. We show that the diffusible inhibitory factor from the NSE-Db thalami is sMHCI. We also show that COS cells programmed to express murine MHCI release sMHCI that inhibits neurite outgrowth from nearby neurons in vitro. The neuroinhibitory effect of sMHCI could be blocked by lowering cAMP levels, suggesting that the neuronal MHCI receptor's signaling mechanism involves a cyclic nucleotide-dependent pathway. Our results suggest that MHCI may not only have neurobiological activity in its membrane-bound form, it may also influence local neurons as a soluble molecule. We discuss the involvement of complement proteins in generating sMHCI and new theoretical models of MHCI's biological activities in the nervous system.

Indexed as

AnimalsChlorocebus aethiopsCoculture TechniquesCOS CellsCulture Media, ConditionedHistocompatibility Antigens Class IMiceMice, Inbred C57BLNeuritesRetinaThalamusCulture Media, ConditionedHistocompatibility Antigens Class I

Identifiers

PMID21483793
PMCPMC3069096
OpenAlexW1968687181

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.