Evidence map›Paper›PMID 22676888›Full record

ArticleJournal of neurotrauma2012

Involvement of mitogen-activated protein kinase pathways in expression of the water channel protein aquaporin-4 after ischemia in rat cortical astrocytes.

Chikako Nito, Hiroshi Kamada, Hidenori Endo, Purnima Narasimhan, Yong-Sun Lee, Pak H Chan

Open access · greenAbstract read
In one paragraph

Article in Journal of neurotrauma, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing 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

34 citing papers in PubMed, 66 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Aquaporins: Gatekeepers of Fluid Dynamics in Traumatic Brain Injury.International journal of molecular sciences · 2024
    Review
  5. Review
  6. Review
  7. "No-reflow" phenomenon in acute ischemic stroke.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024
    Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Ammonia-Induced Glial-Inflammaging.Molecular neurobiology · 2020
    Article
  14. Review
  15. Article
  16. Evidence-based complementary and alternative medicine : eCAM · 2020
    Article
  17. Article
  18. Review
  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

6 authors at 1 institution in 1 country.

Chikako NitoDivision of Neurology, Nephrology, and Rheumatology, Department of Internal Medicine, Nippon Medical School, Tokyo, Japan. cnito@nms.ac.jp
Hiroshi Kamada
Hidenori Endo
Purnima Narasimhan
Yong-Sun Lee
Pak H Chan
Stanford University · US

Funding

Reperfusion and Neurovascular Injury in StrokeR01NS025372 · NINDS · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI CHAN, PAK H · 1988 to 2015
$5.0M
Transgenic Animal CoreP01NS014543 · NINDS · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI CHAN, PAK H · 1985 to 2011
$4.7M
Cell Death/Survival After Global Cerebral IschemiaR01NS038653 · NINDS · STANFORD UNIVERSITY · PI CHAN, PAK H · 1998 to 2013
$4.5M
NINDS NIH HHS P01 NS014543NINDS NIH HHS R01 NS025372NINDS NIH HHS R01 NS038653
6 · The paper itself

Abstract

Brain edema after ischemic brain injury is a key determinant of morbidity and mortality. Aquaporin-4 (AQP4) plays an important role in water transport in the central nervous system and is highly expressed in brain astrocytes. However, the AQP4 regulatory mechanisms are poorly understood. In this study, we investigated whether mitogen-activated protein kinases (MAPKs), which are involved in changes in osmolality, might mediate AQP4 expression in models of rat cortical astrocytes after ischemia. Increased levels of AQP4 in primary cultured astrocytes subjected to oxygen-glucose deprivation (OGD) and 2 h of reoxygenation were observed, after which they immediately decreased at 0 h of reoxygenation. Astrocytes exposed to OGD injury had significantly increased phosphorylation of three kinds of MAPKs. Treatment with SB203580, a selective p38 MAPK inhibitor, or SP600125, a selective c-Jun N-terminal kinase inhibitor, significantly attenuated the return of AQP4 to its normal level, and SB203580, but not SP600125, significantly decreased cell death. In an in vivo study, AQP4 expression was upregulated 1-3 days after reperfusion, which was consistent with the time course of p38 phosphorylation and activation, and decreased by the p38 inhibition after transient middle cerebral artery occlusion (MCAO). These results suggest that p38 MAPK may regulate AQP4 expression in cortical astrocytes after ischemic injury.

Indexed as

AnimalsAnimals, NewbornAquaporin 4AstrocytesCerebral CortexHypoxia-Ischemia, BrainMAP Kinase Signaling Systemp38 Mitogen-Activated Protein KinasesPrimary Cell CultureRatsRats, Sprague-DawleyReperfusion InjuryAqp4 protein, ratAquaporin 4p38 Mitogen-Activated Protein Kinases

Identifiers

PMID22676888
PMCPMC3433694
OpenAlexW2020410632

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.