Evidence map›Paper›PMID 18057239›Full record

ArticleJournal of virology2008

Hippocampal poly(ADP-Ribose) polymerase 1 and caspase 3 activation in neonatal bornavirus infection.

Brent L Williams, Mady Hornig, Kavitha Yaddanapudi, W Ian Lipkin

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

18 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
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  11. Borna disease virus-induced neuronal degeneration dependent on host genetic background and prevented by soluble factors.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Article
  12. Article
  13. Article
  14. Article
  15. Animal models of CNS viral disease: examples from borna disease virus models.Interdisciplinary perspectives on infectious diseases · 2010
    Article
  16. Article
  17. Review
  18. 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

4 authors at 1 institution in 1 country.

Brent L WilliamsCenter for Infection and Immunity, Mailman School of Public Health, Columbia University, 722 West 168th Street, Room 1801, New York, NY 10032, USA. wil2001@columbia.edu
Mady Hornig
Kavitha Yaddanapudi
W Ian Lipkin
Columbia University · US

Funding

A DEVELOPMENTAL MODEL FOR AUTISM BASED ON CNS INFECTIONR01HD037546 · NICHD · UNIVERSITY OF CALIFORNIA IRVINE · PI LIPKIN, W. IAN · 2000 to 2004
$1.8M
MOLECULAR ANALYSIS OF A NEUROTROPIC AGENT--BORNA VIRUSR01NS029425 · NINDS · UNIVERSITY OF CALIFORNIA IRVINE · PI LIPKIN, W. IAN · 1991 to 2002
$1.4M
NICHD NIH HHS HD37546NICHD NIH HHS R01 HD037546NINDS NIH HHS NS29425
6 · The paper itself

Abstract

Infection of neonatal rats with Borna disease virus results in a characteristic behavioral syndrome and apoptosis of subsets of neurons in the hippocampus, cerebellum, and cortex (neonatal Borna disease [NBD]). In the NBD rat hippocampus, dentate gyrus granule cells progressively degenerate. Apoptotic loss of granule cells in NBD is associated with accumulation of zinc in degenerating neurons and reduced zinc in granule cell mossy fibers. Excess zinc can trigger poly(ADP-ribose) polymerase 1 (PARP-1) activation, and PARP-1 activation can mediate neuronal death. Here, we evaluate hippocampal PARP-1 mRNA and protein expression levels, activation, and cleavage, as well as apoptosis-inducing factor (AIF) nuclear translocation and executioner caspase 3 activation, in NBD rats. PARP-1 mRNA and protein levels were increased in NBD hippocampi. PARP-1 expression and activity were increased in granule cell neurons and glia with enhanced ribosylation of proteins, including PARP-1 itself. In contrast, levels of poly(ADP-ribose) glycohydrolase mRNA were decreased in NBD hippocampi. PARP-1 cleavage and AIF expression were also increased in astrocytes in NBD hippocampi. Levels of activated caspase 3 protein were increased in NBD hippocampi and localized to nuclei, mossy fibers, and dendrites of granule cell neurons. These results implicate aberrant zinc homeostasis, PARP-1, and caspase 3 activation as contributing factors in hippocampal neurodegeneration in NBD.

Indexed as

AnimalsAnimals, NewbornApoptosisApoptosis Inducing FactorBorna DiseaseCaspase 3Cerebral CortexDentate GyrusFemaleHippocampusNeurodegenerative DiseasesPoly Adenosine Diphosphate RibosePoly (ADP-Ribose) Polymerase-1Poly(ADP-ribose) PolymerasesRatsRats, Inbred LewApoptosis Inducing FactorCaspase 3Parp1 protein, ratPoly Adenosine Diphosphate RibosePoly (ADP-Ribose) Polymerase-1Poly(ADP-ribose) PolymerasesRNA, MessengerZinc

Identifiers

PMID18057239
PMCPMC2258717
OpenAlexW1983836246

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.