Evidence map›Paper›PMID 24895267›Full record

ArticleGlia2014

The SHH/Gli pathway is reactivated in reactive glia and drives proliferation in response to neurodegeneration-induced lesions.

Kenneth L Pitter, Ilaria Tamagno, Xi Feng, Kaushik Ghosal, Nduka Amankulor, Eric C Holland, Dolores Hambardzumyan

Open access · bronzeAbstract read
In one paragraph

Article in Glia, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

35 citing papers in PubMed, 65 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. Sonic hedgehog signaling in astrocytes.Cellular and molecular life sciences : CMLS · 2021
    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

7 authors at 4 institutions in 1 country.

Kenneth L PitterDepartment of Cancer Biology and Genetics, Memorial Sloan-Kettering Cancer Center, New York, New York; The Brain Tumor Center, Memorial Sloan-Kettering Cancer Center, New York, New York.
Ilaria Tamagno
Xi Feng
Kaushik Ghosal
Nduka Amankulor
Eric C Holland
Dolores Hambardzumyan
Cleveland Clinic · USMemorial Sloan Kettering Cancer Center · USUniversity of Pittsburgh · USUniversity of Washington · US

Funding

Weill Cornell/Rockefeller/Sloan-Kettering MST ProgramT32GM007739 · NIGMS · WEILL MEDICAL COLL OF CORNELL UNIV · PI HSU, KATHARINE C · 1985 to 2023
$51.1M
Non-neoplastic cell types dictate gliomagenesis andU01CA160882 · NCI · EMORY UNIVERSITY · PI HAMBARDZUMYAN, DOLORES, HOLLAND, ERIC C. · 2012 to 2016
$2.8M
Characterizing the functional stem-like properties of primary and recurrent gliomF31NS076028 · NINDS · WEILL MEDICAL COLL OF CORNELL UNIV · PI PITTER, KENNETH L · 2011 to 2013
$141k
NCI NIH HHS U01 CA160882NCI NIH HHS U01-CA160882NIGMS NIH HHS T32 GM007739NINDS NIH HHS F31 NS076028NINDS NIH HHS NS076028
6 · The paper itself

Abstract

In response to neurodegeneration, the adult mammalian brain activates a cellular cascade that results in reactive astrogliosis and microgliosis. The mechanism through which astrocytes become reactive and the physiological consequences of their activation in response to neurodegeneration is complex. While the activation and proliferation of astrocytes has been shown to occur during massive neuronal cell death, the functional relationship between these two events has not been clearly elucidated. Here we show that in response to kainic acid- (KA) induced neurodegeneration, the mitogen sonic hedgehog (SHH) is upregulated in reactive astrocytes. SHH activity peaks at 7 days and is accompanied by increased Gli activity and elevated proliferation in several cell types. To determine the functional role of SHH-Gli signaling following KA lesions, we used a pharmacological approach to show that SHH secreted by astrocytes drives the activation and proliferation of astrocytes and microglia. The consequences of SHH-Gli signaling in KA-induced lesions appear to be independent of the severity of neurodegeneration.

Indexed as

AnimalsAstrocytesCell ProliferationCentral Nervous System AgentsDisease Models, AnimalHedgehog ProteinsHippocampusKainic AcidKruppel-Like Transcription FactorsMiceMice, TransgenicMicrogliaNeurodegenerative DiseasesNeurogenesisNeuronsSeizuresCentral Nervous System AgentscyclopamineGli1 protein, mouseHedgehog ProteinsKainic AcidKruppel-Like Transcription FactorsShh protein, mouseVeratrum AlkaloidsZinc Finger Protein GLI1astrogliosisGlimicrogliosisneurodegenerationSonic Hedgehog

Identifiers

PMID24895267
PMCPMC4489138
OpenAlexW1544587770

What OpenQuestion holds

Textmetadata
LicenceTDM
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.