Evidence map›Paper›PMID 21797866›Full record

ArticleJournal of neurochemistry2011

Role of sodium/hydrogen exchanger isoform 1 in microglial activation and proinflammatory responses in ischemic brains.

Yejie Shi, Vishal Chanana, Jyoti J Watters, Peter Ferrazzano, Dandan Sun

Open access · greenAbstract read
In one paragraph

Article in Journal of neurochemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 2 pooled it
4.3field-weighted citation impact, top 7% 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

41 citing papers in PubMed, 2 syntheses or guidelines pooled it, 63 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Inhibition of NaJournal of neural engineering · 2021
    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

5 authors at 2 institutions in 1 country.

Yejie ShiDepartment of Neurological Surgery, University of Wisconsin, Madison, Wisconsin, USA.
Vishal Chanana
Jyoti J Watters
Peter Ferrazzano
Dandan Sun
University of Wisconsin–Madison · USNeurological Surgery · US

Funding

WISCONSIN CENTER ON MENTAL RETARDATION: CORE SUPPORTP30HD003352 · NICHD · UNIVERSITY OF WISCONSIN-MADISON · PI MESSING, ALBEE · 1985 to 2015
$25.2M
The Role of Na+/H+ exchanger in Cerebral IschemiaR01NS048216 · NINDS · UNIVERSITY OF WISCONSIN-MADISON · PI Dandan Sun · 2005 to 2026
$6.1M
Na-K-Cl Contransporter in Cerebral IschemiaR01NS038118 · NINDS · UNIVERSITY OF WISCONSIN-MADISON · PI SUN, DANDAN · 2000 to 2018
$5.0M
Microglia adenine nucleotides and hypoxiaR01NS049033 · NINDS · UNIVERSITY OF WISCONSIN-MADISON · PI WATTERS, JYOTI J · 2005 to 2009
$1.3M
NICHD NIH HHS P30 HD003352NICHD NIH HHS P30 HD03352NINDS NIH HHS R01 NS038118NINDS NIH HHS R01 NS048216NINDS NIH HHS R01 NS049033NINDS NIH HHS R01 NS38118NINDS NIH HHS R01 NS48216NINDS NIH HHS R01 NS49033
6 · The paper itself

Abstract

Our recent study reveals that Na⁺/H⁺ exchanger isoform 1 (NHE-1) mediates H⁺ extrusion during "respiratory bursting", which is important for microglial activation. In the present study, we further investigated whether NHE-1 plays a role in proinflammatory activation of microglia in vivo using a mouse model of transient focal cerebral ischemia and reperfusion (I/R). Activated microglial cells were identified by their expression of two microglial marker proteins (CD11b and Iba1) as well as by their transformation from a "ramified" to an "amoeboid" morphology. An immediate increase in activated microglial numbers was detected in the ipsilateral ischemic core area of NHE-1⁺/⁺ brains at 1 hour (h) I/1 h R, which gradually decreased during 6-24 h I/R. This was followed by a sharp rise in microglial activation in the peri-infarct area and an increase in proinflammatory cytokine formation at 3 day after I/R. Interestingly, HOE 642 (a potent NHE-1 inhibitor) -treated or NHE-1 heterozygous (NHE-1⁺/⁻) mice exhibited less microglia activation, less NADPH oxidase activation, or a reduced proinflammatory response at 3-7 day after I/R. Blocking NHE-1 activity also significantly decreased microglial phagocytosis in vitro. In contrast, astrogliosis formation in the peri-infarct area was not affected by NHE-1 inhibition. Taken together, our results demonstrate that NHE-1 protein was abundantly expressed in activated microglia and astrocytes. NHE-1 inhibition reduced microglial proinflammatory activation following ischemia.

Indexed as

AnimalsBrain IschemiaCation Transport ProteinsCells, CulturedCerebral InfarctionCytokinesEnzyme InhibitorsFluorescent Antibody TechniqueGliosisGlucoseGuanidinesHypoxia, BrainInflammationMacrophage ActivationMiceMice, KnockoutcariporideCation Transport ProteinsCytokinesEnzyme InhibitorsGlucoseGuanidinesNADPH OxidasesSlc9a1 protein, mouseSodium-Hydrogen Exchanger 1Sodium-Hydrogen ExchangersSulfonesTetrazolium Saltstriphenyltetrazolium

Identifiers

PMID21797866
PMCPMC3192493
OpenAlexW1583452713

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.