GPR124 Alleviates Blood-Brain Barrier Disruption by Enhancing Microvascular Endothelial Function after Traumatic Brain Injury.
Overview
- Department of Neurosurgery, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China
- School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, China
Abstract
Traumatic brain injury (TBI) is a leading cause of death among young adults worldwide. However, the role of G protein‐coupled receptor 124 (GPR124), a key regulator of the nervous system, in TBI remains unexplored. We employed a controlled cortical impact (CCI) model combined with single‐cell RNA sequencing to analyze the localization of GPR124 expression following TBI. Additionally, we used mice with endothelial cell (EC)‐specific conditional knockout (CKO) of GPR124 to perform behavioral experiments. A stretch injury (SI) model was also established to investigate the effects of GPR124 on ECs. Neurological recovery after TBI was significantly impaired in mice with the EC‐specific CKO of GPR124. Furthermore, GPR124 knockdown reduced EC function after SI. Notably, tight junction integrity was disrupted both in vivo and in vitro after GPR124 knockdown. Mass spectrometry and immunoprecipitation analyses confirmed that GPR124 interacts with fibroblast growth factor binding protein‐1, thereby activating the Wnt/
Reproduced under the paper's license (CC BY), from the paper cited above.
Code
The paper links to its data, not to its authors' code: see the Data section.
Tracing map
A tracing map links a paper to the code its authors published: this paper has none, so it has no map.
Data
Datasets cited
- geo:GSE302863 — at NCBI GEO; found in “Data Availability Statement”
Data Availability Statement
The scRNAseq data have been deposited in Gene Expression Omnibus. (GSE302863 (https://
Reproduced under the paper's license (CC BY), from the paper cited above.
Versions
The history of this record: each version stored by the harvester or made by a correction of its authors or of the maintainers of its code, and what changed in its facts. The texts of the paper (its abstract, its availability statements) are not part of it; versions that changed only those are not listed.
Version 1, 27 September 2026: the first record
Recorded: type, language, journal, volume, issue, pages, dates, 14 authors, 5 keywords, 11 MeSH terms, 4 funders, 37 references.
Cite
This paper
Wang, C., Cai, L., Gong, Q., Yang, Y., Liang, Y., Niu, X., Wei, L., Liu, Z., Wu, S., Men, Y., Tang, Y., Ding, J., Tian, H., & Chen, H. (2026). GPR124 Alleviates Blood-Brain Barrier Disruption by Enhancing Microvascular Endothelial Function after Traumatic Brain Injury. Advanced science (Weinheim, Baden-Wurttemberg, Germany), 13(51), e01197. https://
BibTeX
@article{wang2026gpr124,
author = {Wang, Chen and Cai, Lin and Gong, Qiuyuan and Yang, Yang and Liang, Yuqing and Niu, Xinyu and Wei, Lai and Liu, Ze and Wu, Shengju and Men, Yinghui and Tang, Yaohui and Ding, Jun and Tian, Hengli and Chen, Hao},
title = {{GPR124 Alleviates Blood-Brain Barrier Disruption by Enhancing Microvascular Endothelial Function after Traumatic Brain Injury}},
journal = {Advanced science (Weinheim, Baden-Wurttemberg, Germany)},
year = {2026},
month = jun,
volume = {13},
number = {51},
pages = {e01197},
publisher = {Wiley},
issn = {2198-3844},
doi = {10.1002/
url = {https://
pmid = {42294584},
pmcid = {PMC13336676}
}
RIS
TY - JOUR
AU - Wang, Chen
AU - Cai, Lin
AU - Gong, Qiuyuan
AU - Yang, Yang
AU - Liang, Yuqing
AU - Niu, Xinyu
AU - Wei, Lai
AU - Liu, Ze
AU - Wu, Shengju
AU - Men, Yinghui
AU - Tang, Yaohui
AU - Ding, Jun
AU - Tian, Hengli
AU - Chen, Hao
TI - GPR124 Alleviates Blood-Brain Barrier Disruption by Enhancing Microvascular Endothelial Function after Traumatic Brain Injury
T2 - Advanced science (Weinheim, Baden-Wurttemberg, Germany)
J2 - Adv Sci (Weinh)
PY - 2026
DA - 2026/
VL - 13
IS - 51
SP - e01197
SN - 2198-3844
PB - Wiley
DO - 10.1002/
UR - https://
LA - en
ER -
CSL-JSON
{
"id": "10.1002/
"type": "article-journal",
"title": "GPR124 Alleviates Blood-Brain Barrier Disruption by Enhancing Microvascular Endothelial Function after Traumatic Brain Injury",
"container-title": "Advanced science (Weinheim, Baden-Wurttemberg, Germany)",
"author": [
{
"family": "Wang",
"given": "Chen"
},
{
"family": "Cai",
"given": "Lin"
},
{
"family": "Gong",
"given": "Qiuyuan"
},
{
"family": "Yang",
"given": "Yang"
},
{
"family": "Liang",
"given": "Yuqing"
},
{
"family": "Niu",
"given": "Xinyu"
},
{
"family": "Wei",
"given": "Lai"
},
{
"family": "Liu",
"given": "Ze"
},
{
"family": "Wu",
"given": "Shengju"
},
{
"family": "Men",
"given": "Yinghui"
},
{
"family": "Tang",
"given": "Yaohui"
},
{
"family": "Ding",
"given": "Jun"
},
{
"family": "Tian",
"given": "Hengli"
},
{
"family": "Chen",
"given": "Hao"
}
],
"container-title-short":
"volume": "13",
"issue": "51",
"page": "e01197",
"DOI": "10.1002/
"PMID": "42294584",
"PMCID": "PMC13336676",
"ISSN": "2198-3844",
"publisher": "Wiley",
"URL": "https://
"language": "en",
"issued": {
"date-parts": [
[
2026,
6,
15
]
]
}
}
Similar papers
The papers with a page that share the most with this one: the tools found in their code, their categories, datasets, cited references and authors, the rarest counting most.
- [1] doi:10.1038/s41467-026-75367-0
- Heterogenous microglial reactivity contrasts with stable vascular transcriptional programs in mouse models of Alzheimer's, CADASIL, and Traumatic Brain Injury.Journal: Nature communicationsIn common: traumatic brain injury, mouse, cellular / molecular, 2 references
- [2] doi:10.1186/s12987-026-00840-3
- Spatiotemporal arising of molecular and functional blood-brain barrier properties in the developing Gallus gallus optic tectum.Journal: Fluids and barriers of the CNSIn common: 2 references
- [3] doi:10.1172/jci196112
- Aging-dependent microglial heterogeneity worsens outcomes in models of traumatic brain injury.Journal: The Journal of clinical investigationIn common: traumatic brain injury, mouse, 1 reference
- [4] doi:10.3389/fimmu.2026.1867920
- A self-perpetuating neuron-intrinsic GSDMD-mtDNA-AIM2 inflammasome axis drives neuronal pyroptosis and cognitive impairment after traumatic brain injury.Journal: Frontiers in immunologyIn common: traumatic brain injury, mouse, cellular / molecular, 1 reference
- [5] doi:10.1186/s12974-026-03890-4 [code]
- Neuronal toll-like receptor-4 regulation of matrix metalloproteinase-9 activity mediates dentate circuit dysfunction after traumatic brain injury.Journal: Journal of neuroinflammationIn common: traumatic brain injury, mouse, cellular / molecular, 1 reference
- [6] doi:10.3390/ijms27146143
- Integrated WGCNA and Network Pharmacology Explore the Potential Mechanisms of D-Limonene in Alleviating Traumatic Brain Injury.Journal: International journal of molecular sciencesIn common: traumatic brain injury, cellular / molecular, 1 reference
- [7] doi:10.1503/cmaj.251721 [code]
- Differences in admission to trauma centres by sex among adults with traumatic brain injury: a population-based cohort study.Journal: CMAJ : Canadian Medical Association journal = journal de l'Association medicale canadienneIn common: traumatic brain injury, 1 reference
- [8] doi:10.3389/fcell.2026.1876873
- Multi-omics integration reveals TIM-4 as a master regulatory hub of neuroinflammation and neuronal cell death.Journal: Frontiers in cell and developmental biologyIn common: traumatic brain injury, cellular / molecular, 1 reference
- [9] doi:10.1016/j.xcrm.2026.102867
- Psilocybin restores behavior and 5-HT&
lt;sub& gt;2A& lt;/ sub& gt; signaling while reducing microglial density after chronic traumatic brain injury in rats. Journal: Cell reports. MedicineIn common: traumatic brain injury, cellular / molecular, 1 reference - [10] doi:10.1002/cbf.70231
- Neuroglial Response to High-Amplitude, Short-Duration Pressure Transients in Monoculture.Journal: Cell biochemistry and functionIn common: traumatic brain injury, cellular / molecular, 1 reference
Contribute
The authors of this paper can claim it, correct its record and validate its tracing map, and the maintainers of its code (its owner, or a public member of its organization) correct what it says of their repository; anyone signed in can ask for its removal. Every request goes to OSCR's own machine, which answers it; your account page follows them.
Sign in with ORCID to claim this paper as one of its authors, correct its record or validate its tracing map: when the paper's metadata lists your ORCID iD, you are recognized at once. Maintainers of its code: sign in with GitHub, then claim the repository on your account page.
Claim this paper
Correct its record
Say what each link of this record is, remove the ones that are not the paper's, add the ones that are missing. The correction becomes a new version of the record, in its Versions section.
Request its removal
To ask OSCR to remove this record, the copies of its authors' scripts or its tracing map, use the removal request page: signed in, you say who you are, what to remove and why, then review and confirm the request. Published rules decide every request (how).
Discussion, reproductions, activity
Discussion: questions and error reports about this paper and its code, from signed-in readers and its authors. It opens with sign-in.
Reproductions: reports from readers who ran the authors' code: what they reproduced, with which environment, commit and data. It opens with sign-in.
Activity: what happens around this paper: new versions of its record, its map's validation, discussions and reproductions. It opens with sign-in.