Evidence map›Paper›PMID 36245918›Full record

ArticleFrontiers in molecular neuroscience2022

Extracellular signal-regulated kinase-dependent phosphorylation of histone H3 serine 10 is involved in the pathogenesis of traumatic brain injury.

Yu Zhang, Xin Yang, Xinran Hou, Wen Zhou, Changlong Bi, Zhuanyi Yang, Sining Lu, Zijin Ding, Zhuofeng Ding, Yu Zou and 3 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in molecular neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.5field-weighted citation impact, top 34% 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

3 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
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.

Yu ZhangDepartment of Anesthesiology, Xiangya Hospital Central South University, Changsha, China.
Xin YangDepartment of Anesthesiology, Xiangya Hospital Central South University, Changsha, China.
Xinran HouDepartment of Anesthesiology, Xiangya Hospital Central South University, Changsha, China.
Wen ZhouDepartment of Anesthesiology, Xiangya Hospital Central South University, Changsha, China.
Changlong BiDepartment of Neurosurgery, Xiangya Hospital Central South University, Changsha, China.
Zhuanyi YangDepartment of Neurosurgery, Xiangya Hospital Central South University, Changsha, China.
Sining LuMedical College of Xiangya, Central South University, Changsha, China.
Zijin DingDepartment of Anesthesiology, Xiangya Hospital Central South University, Changsha, China.
Zhuofeng DingDepartment of Anesthesiology, Xiangya Hospital Central South University, Changsha, China.
Yu ZouDepartment of Anesthesiology, Xiangya Hospital Central South University, Changsha, China.
Qulian GuoDepartment of Anesthesiology, Xiangya Hospital Central South University, Changsha, China.
Michael K E SchäferDepartment of Anesthesiology, University Medical Center, Johannes Gutenberg University Mainz, Mainz, Germany.
Changsheng HuangDepartment of Anesthesiology, Xiangya Hospital Central South University, Changsha, China.
Xiangya Hospital Central South University · CNCentral South University · CNJohannes Gutenberg University Mainz · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Traumatic brain injury (TBI) induces a series of epigenetic changes in brain tissue, among which histone modifications are associated with the deterioration of TBI. In this study, we explored the role of histone H3 modifications in a weight-drop model of TBI in rats. Screening for various histone modifications, immunoblot analyses revealed that the phosphorylation of histone H3 serine 10 (p-H3S10) was significantly upregulated after TBI in the brain tissue surrounding the injury site. A similar posttraumatic regulation was observed for phosphorylated extracellular signal-regulated kinase (p-ERK), which is known to phosphorylate H3S10. In support of the hypothesis that ERK-mediated phosphorylation of H3S10 contributes to TBI pathogenesis, double immunofluorescence staining of brain sections showed high levels and colocalization of p-H3S10 and p-ERK predominantly in neurons surrounding the injury site. To test the hypothesis that inhibition of ERK-H3S10 signaling ameliorates TBI pathogenesis, the mitogen-activated protein kinase-extracellular signal-regulated kinase kinase (MEK) 1/2 inhibitor U0126, which inhibits ERK phosphorylation, was administered into the right lateral ventricle of TBI male and female rats via intracerebroventricular cannulation for 7 days post trauma. U0126 administration indeed prevented H3S10 phosphorylation and improved motor function recovery and cognitive function compared to vehicle treatment. In agreement with our findings in the rat model of TBI, immunoblot and double immunofluorescence analyses of brain tissue specimens from patients with TBI demonstrated high levels and colocalization of p-H3S10 and p-ERK as compared to control specimens from non-injured individuals. In conclusion, our findings indicate that phosphorylation-dependent activation of ERK-H3S10 signaling participates in the pathogenesis of TBI and can be targeted by pharmacological approaches.

Indexed as

ERKH3S10histone modificationphosphorylationtraumatic brain injury

Identifiers

PMID36245918
PMCPMC9557206
OpenAlexW4298001186

What OpenQuestion holds

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LicenceCC BY
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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.