Evidence map›Paper›PMID 19628872›Full record

ArticleThe Journal of biological chemistry2009

PARP-1 deficiency increases the severity of disease in a mouse model of multiple sclerosis.

Vimal Selvaraj, Mangala M Soundarapandian, Olga Chechneva, Ambrose J Williams, Maxim K Sidorov, Athena M Soulika, David E Pleasure, Wenbin Deng

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

21 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Modulation of PARP activity by Monomethylarsonous (MMAToxicology and applied pharmacology · 2021
    Article
  8. Evaluation of the NADExperimental neurology · 2020
    Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Review
  17. Article
  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

8 authors at 3 institutions in 2 countries.

Vimal SelvarajDepartment of Cell Biology and Human Anatomy, School of Medicine, University of California, Davis, Sacramento, California 95817, USA.
Mangala M Soundarapandian
Olga Chechneva
Ambrose J Williams
Maxim K Sidorov
Athena M Soulika
David E Pleasure
Wenbin Deng
Institute of Cell Biology and Neurobiology · ITShriners Hospitals for Children - Northern California · USUniversity of California, Davis · US

Funding

OLIGODENDROGLIAL PROLIFERATION AND DIFFERENTIATIONR01NS025044 · NINDS · UNIVERSITY OF CALIFORNIA DAVIS · PI PLEASURE, DAVID E. · 1987 to 2011
$3.9M
Oligodendrocytes, Glutamate Receptors, and Lead NeurotoxicityR01ES015988 · NIEHS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI DENG, WENBIN · 2007 to 2011
$2.0M
Glutamate Receptors in Hypoxic-ischemic Injury to Developing OligodendrocytesR01NS059043 · NINDS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI DENG, WENBIN · 2008 to 2012
$1.4M
NIEHS NIH HHS R01 ES015988NINDS NIH HHS R01 NS025044NINDS NIH HHS R01 NS059043
6 · The paper itself

Abstract

Poly(ADP-ribose) polymerase-1 (PARP-1) has been implicated in the pathogenesis of several central nervous system (CNS) disorders. However, the role of PARP-1 in autoimmune CNS injury remains poorly understood. Therefore, we studied experimental autoimmune encephalomyelitis (EAE), a model for multiple sclerosis in mice with a targeted deletion of PARP-1. We identified inherent physiological abnormalities in the circulating and splenic immune composition between PARP-1(-/-) and wild type (WT) mice. Upon EAE induction, PARP-1(-/-) mice had an earlier onset and developed a more severe EAE compared with WT cohorts. Splenic response was significantly higher in PARP-1(-/-) mice largely because of B cell expansion. Although formation of Th1 and Th17 effector T lymphocytes was unaffected, PARP-1(-/-) mice had significantly earlier CD4+ T lymphocyte and macrophage infiltration into the CNS during EAE. However, we did not detect significant differences in cytokine profiles between PARP-1(-/-) and WT spinal cords at the peak of EAE. Expression analysis of different PARP isozymes in EAE spinal cords showed that PARP-1 was down-regulated in WT mice and that PARP-3 but not PARP-2 was dramatically up-regulated in both PARP-1(-/-) and WT mice, suggesting that these PARP isozymes could have distinct roles in different CNS pathologies. Together, our results indicate that PARP-1 plays an important role in regulating the physiological immune composition and in immune modulation during EAE; our finding identifies a new aspect of immune regulation by PARPs in autoimmune CNS pathology.

Indexed as

Poly(ADP-ribose) PolymerasesAnimalsEncephalomyelitis, Autoimmune, ExperimentalGene Expression Regulation, EnzymologicIsoenzymesMacrophagesMiceMice, KnockoutMultiple SclerosisPoly (ADP-Ribose) Polymerase-1Spinal CordTh1 CellsUp-RegulationIsoenzymesParp1 protein, mouseParp2 protein, mousePoly (ADP-Ribose) Polymerase-1Poly(ADP-ribose) Polymerases

Identifiers

PMID19628872
PMCPMC2758007
OpenAlexW1970910000

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.