Evidence map›Paper›PMID 35942676›Full record

ArticleeLife2022

Lactate receptor HCAR1 regulates neurogenesis and microglia activation after neonatal hypoxia-ischemia.

Lauritz Kennedy, Emilie R Glesaaen, Vuk Palibrk, Marco Pannone, Wei Wang, Ali Al-Jabri, Rajikala Suganthan, Niklas Meyer, Marie Landa Austbø, Xiaolin Lin and 3 more

Open access · goldAbstract read
In one paragraph

Article in eLife, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
23.2field-weighted citation impact, top 1% 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

43 citing papers in PubMed, 66 citations in OpenAlex.

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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

13 authors at 3 institutions in 2 countries.

Lauritz Kennedy *Department of Microbiology, Oslo University Hospital and University of Oslo, Oslo, Norway.
Emilie R Glesaaen *Department of Microbiology, Oslo University Hospital and University of Oslo, Oslo, Norway.
Vuk PalibrkDepartment of Clinical and Molecular Medicine, Norwegian University of Science and Technology, Trondheim, Norway.
Marco PannoneDepartment of Microbiology, Oslo University Hospital and University of Oslo, Oslo, Norway.
Wei WangDepartment of Clinical and Molecular Medicine, Norwegian University of Science and Technology, Trondheim, Norway.
Ali Al-JabriDepartment of Microbiology, Oslo University Hospital and University of Oslo, Oslo, Norway.
Rajikala SuganthanDepartment of Microbiology, Oslo University Hospital and University of Oslo, Oslo, Norway.
Niklas MeyerDepartment of Microbiology, Oslo University Hospital and University of Oslo, Oslo, Norway.ORCID 0000-0002-8377-097X
Marie Landa AustbøDepartment of Microbiology, Oslo University Hospital and University of Oslo, Oslo, Norway.
Xiaolin LinDepartment of Microbiology, Oslo University Hospital and University of Oslo, Oslo, Norway.
Linda H BergersenThe Brain and Muscle Energy Group, Institute of Oral Biology, Faculty of Dentistry, University of Oslo, Oslo, Norway.
Magnar Bjørås *Department of Microbiology, Oslo University Hospital and University of Oslo, Oslo, Norway.
Johanne E Rinholm *Department of Microbiology, Oslo University Hospital and University of Oslo, Oslo, Norway.ORCID 0000-0003-3741-850X
Oslo University Hospital · NONorwegian University of Science and Technology · NOUniversity of Copenhagen · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neonatal cerebral hypoxia-ischemia (HI) is the leading cause of death and disability in newborns with the only current treatment being hypothermia. An increased understanding of the pathways that facilitate tissue repair after HI may aid the development of better treatments. Here, we study the role of lactate receptor HCAR1 in tissue repair after neonatal HI in mice. We show that HCAR1 knockout mice have reduced tissue regeneration compared with wildtype mice. Furthermore, proliferation of neural progenitor cells and glial cells, as well as microglial activation was impaired. Transcriptome analysis showed a strong transcriptional response to HI in the subventricular zone of wildtype mice involving about 7300 genes. In contrast, the HCAR1 knockout mice showed a modest response, involving about 750 genes. Notably, fundamental processes in tissue repair such as cell cycle and innate immunity were dysregulated in HCAR1 knockout. Our data suggest that HCAR1 is a key transcriptional regulator of pathways that promote tissue regeneration after HI.

Indexed as

Lactic AcidMicrogliaAnimalsAnimals, NewbornBrainHypoxiaIschemiaMiceMice, KnockoutNeurogenesisReceptors, G-Protein-CoupledHcar1 protein, mouseLactic AcidReceptors, G-Protein-Coupledcell biologygpr81hca1hcar1ischemialactatemouseneurogenesisneuroscience

Identifiers

PMID35942676
PMCPMC9363115
OpenAlexW4291020820

What OpenQuestion holds

Textmetadata
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.