Evidence map›Paper›PMID 22867428›Full record

ArticleASN neuro2012

Mice lacking the β2 adrenergic receptor have a unique genetic profile before and after focal brain ischaemia.

Robin E White, Curtis Palm, Lijun Xu, Evelyn Ling, Mitchell Ginsburg, Bernie J Daigle, Ruquan Han, Andrew Patterson, Russ B Altman, Rona G Giffard

Open access · goldAbstract read
In one paragraph

Article in ASN neuro, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 17% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Implication of Central βArchiv der Pharmazie · 2025
    Review
  5. Neuroprotective actions of norepinephrine in neurological diseases.Pflugers Archiv : European journal of physiology · 2024
    Review
  6. Article
  7. Article
  8. Ras-like Gem GTPase induced by Npas4 promotes activity-dependent neuronal tolerance for ischemic stroke.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
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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

10 authors at 1 institution in 1 country.

Robin E White*Department of Anesthesia, Stanford University, 300 Pasteur Drive, Grant Building S282, Stanford, CA 94305, U.S.A.
Curtis Palm†Genome Technology Center, Stanford University, 855 S. California Avenue, Palo Alto, CA 94305, U.S.A.
Lijun Xu*Department of Anesthesia, Stanford University, 300 Pasteur Drive, Grant Building S282, Stanford, CA 94305, U.S.A.
Evelyn Ling*Department of Anesthesia, Stanford University, 300 Pasteur Drive, Grant Building S282, Stanford, CA 94305, U.S.A.
Mitchell Ginsburg*Department of Anesthesia, Stanford University, 300 Pasteur Drive, Grant Building S282, Stanford, CA 94305, U.S.A.
Bernie J Daigle‡Department of Computer Science, University of California Santa Barbara, Santa Barbara, CA 931065070, U.S.A.
Ruquan Han
Andrew Patterson*Department of Anesthesia, Stanford University, 300 Pasteur Drive, Grant Building S282, Stanford, CA 94305, U.S.A.
Russ B Altman¶Department of Bioengineering, Stanford University, 318 Campus Drive S172, Stanford, CA 94305, U.S.A.
Rona G Giffard*Department of Anesthesia, Stanford University, 300 Pasteur Drive, Grant Building S282, Stanford, CA 94305, U.S.A.
Beijing Tian Tan Hospital · CN

Funding

POSTDOCTORAL TRAINING IN MEDICAL INFORMATION SCIENCEST15LM007033 · NLM · STANFORD UNIVERSITY · PI SYLVIA KATINA PLEVRITIS · 1985 to 2026
$25.5M
PharmGKB: pharmacogenomics knowledge for precision medicineR24GM061374 · NIGMS · STANFORD UNIVERSITY · PI ALTMAN, RUSS BIAGIO, KLEIN, TERI ELLEN · 2010 to 2018
$25.2M
THE STANFORD PHARMACOGENETICS KNOWLEDGE BASEU01GM061374 · NIGMS · STANFORD UNIVERSITY · PI ALTMAN, RUSS BIAGIO · 2000 to 2009
$24.0M
Research in Anesthesia Training Program (ReAP)T32GM089626 · NIGMS · STANFORD UNIVERSITY · PI Vivianne L Tawfik · 2010 to 2026
$5.2M
ANESTHETICS AND STRESS PROTEINS IN BRAIN CELL INJURYR01GM049831 · NIGMS · STANFORD UNIVERSITY · PI GIFFARD, RONA G · 1993 to 2011
$4.1M
NIGMS NIH HHS GM49831NIGMS NIH HHS GM61374NIGMS NIH HHS R01 GM049831NIGMS NIH HHS R24 GM061374NIGMS NIH HHS T32 GM089626NIGMS NIH HHS T32GM089626NIGMS NIH HHS U01 GM061374NLM NIH HHS T15 LM007033
6 · The paper itself

Abstract

The role of the β2AR (β2 adrenergic receptor) after stroke is unclear as pharmacological manipulations of the β2AR have produced contradictory results. We previously showed that mice deficient in the β2AR (β2KO) had smaller infarcts compared with WT (wild-type) mice (FVB) after MCAO (middle cerebral artery occlusion), a model of stroke. To elucidate mechanisms of this neuroprotection, we evaluated changes in gene expression using microarrays comparing differences before and after MCAO, and differences between genotypes. Genes associated with inflammation and cell deaths were enriched after MCAO in both genotypes, and we identified several genes not previously shown to increase following ischaemia (Ccl9, Gem and Prg4). In addition to networks that were similar between genotypes, one network with a central core of GPCR (G-protein-coupled receptor) and including biological functions such as carbohydrate metabolism, small molecule biochemistry and inflammation was identified in FVB mice but not in β2KO mice. Analysis of differences between genotypes revealed 11 genes differentially expressed by genotype both before and after ischaemia. We demonstrate greater Glo1 protein levels and lower Pmaip/Noxa mRNA levels in β2KO mice in both sham and MCAO conditions. As both genes are implicated in NF-κB (nuclear factor κB) signalling, we measured p65 activity and TNFα (tumour necrosis factor α) levels 24 h after MCAO. MCAO-induced p65 activation and post-ischaemic TNFα production were both greater in FVB compared with β2KO mice. These results suggest that loss of β2AR signalling results in a neuroprotective phenotype in part due to decreased NF-κB signalling, decreased inflammation and decreased apoptotic signalling in the brain.

Indexed as

AnimalsBrain IschemiaCell DeathCytokinesGene Expression RegulationGene Regulatory NetworksMaleMiceMice, KnockoutMicroarray AnalysisNerve Tissue ProteinsNF-kappa BProto-Oncogene Proteins c-bcl-2rab GTP-Binding ProteinsReceptors, Adrenergic, beta-2Receptors, G-Protein-CoupledCytokinesNerve Tissue ProteinsNF-kappa BPmaip1 protein, mouseProto-Oncogene Proteins c-bcl-2rab GTP-Binding ProteinsReceptors, Adrenergic, beta-2Receptors, G-Protein-CoupledRNA, MessengerTumor Necrosis Factor-alpha

Identifiers

PMID22867428
PMCPMC3436074
OpenAlexW2065532910

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.