Evidence map›Paper›PMID 25620910›Full record

ArticleFrontiers in cellular neuroscience2014

CHIP, a carboxy terminus HSP-70 interacting protein, prevents cell death induced by endoplasmic reticulum stress in the central nervous system.

Felipe Cabral Miranda, Juliana Adão-Novaes, William W Hauswirth, Rafael Linden, Hilda Petrs-Silva, Luciana B Chiarini

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cellular neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.6field-weighted citation impact, top 19% 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

15 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. CHIP ameliorates neuronal damage in HScientific reports · 2022
    Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. rAAV8-733-Mediated Gene Transfer of CHIP/Stub-1 Prevents Hippocampal Neuronal Death in Experimental Brain Ischemia.Molecular therapy : the journal of the American Society of Gene Therapy · 2017
    Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Regulation of autophagic flux by CHIP.Neuroscience bulletin · 2015
    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

6 authors at 1 institution in 1 country.

Felipe Cabral MirandaLaboratório de Neurogênese, Departamento de Neurobiologia, Instituto de Biofísica Carlos Chagas Filho, Universidade Federal Do Rio de Janeiro Rio de Janeiro, Brazil.
Juliana Adão-NovaesLaboratório de Neurogênese, Departamento de Neurobiologia, Instituto de Biofísica Carlos Chagas Filho, Universidade Federal Do Rio de Janeiro Rio de Janeiro, Brazil.
William W HauswirthRetinal Gene Therapy Group, Department of Ophthalmology, University of Florida Gainesville, FL, USA.
Rafael LindenLaboratório de Neurogênese, Departamento de Neurobiologia, Instituto de Biofísica Carlos Chagas Filho, Universidade Federal Do Rio de Janeiro Rio de Janeiro, Brazil.
Hilda Petrs-SilvaLaboratório de Neurogênese, Departamento de Neurobiologia, Instituto de Biofísica Carlos Chagas Filho, Universidade Federal Do Rio de Janeiro Rio de Janeiro, Brazil.
Luciana B ChiariniLaboratório de Neurogênese, Departamento de Neurobiologia, Instituto de Biofísica Carlos Chagas Filho, Universidade Federal Do Rio de Janeiro Rio de Janeiro, Brazil.
University of Florida · US

Funding

Vision Research CoreP30EY021721 · NEI · UNIVERSITY OF FLORIDA · PI HAUSWIRTH, WILLIAM W · 2011 to 2015
$2.8M
NEI NIH HHS P30 EY021721
6 · The paper itself

Abstract

Endoplasmic reticulum (ER) stress and protein misfolding are associated with various neurodegenerative diseases. ER stress activates unfolded protein response (UPR), an adaptative response. However, severe ER stress can induce cell death. Here we show that the E3 ubiquitin ligase and co-chaperone Carboxyl Terminus HSP70/90 Interacting Protein (CHIP) prevents neuron death in the hippocampus induced by severe ER stress. Organotypic hippocampal slice cultures (OHSCs) were exposed to Tunicamycin, a pharmacological ER stress inducer, to trigger cell death. Overexpression of CHIP was achieved with a recombinant adeno-associated viral vector (rAAV) and significantly diminished ER stress-induced cell death, as shown by analysis of propidium iodide (PI) uptake, condensed chromatin, TUNEL and cleaved caspase 3 in the CA1 region of OHSCs. In addition, overexpression of CHIP prevented upregulation of both CHOP and p53 both pro-apoptotic pathways induced by ER stress. We also detected an attenuation of eIF2a phosphorylation promoted by ER stress. However, CHIP did not prevent upregulation of BiP/GRP78 induced by UPR. These data indicate that overexpression of CHIP attenuates ER-stress death response while maintain ER stress adaptative response in the central nervous system. These results indicate a neuroprotective role for CHIP upon UPR signaling. CHIP emerge as a candidate for clinical intervention in neurodegenerative diseases associated with ER stress.

Indexed as

AAV-vectorsCHIPER stressHippocampusneurodegenerationUPR signaling pathways

Identifiers

PMID25620910
PMCPMC4288139
OpenAlexW1968394233

What OpenQuestion holds

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LicenceCC BY
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.