Evidence map›Paper›PMID 42682555›Full record

ArticleFrontiers in cellular neuroscience2026

Single-cell transcriptomics identifies a putative perivascular macrophage-endothelial MIF-ACKR3 axis associated with endothelial activation in acute traumatic brain injury.

Yanya Lin, Chengda Lin, Jianhui Chen, Shijun Chen, Jianhuang Huang, Jianxiong Hu

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Article in Frontiers in cellular neuroscience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Yanya LinThe Graduate School of Fujian Medical University, Fuzhou, Fujian, China.
Chengda LinDepartment of Neurosurgery, Putian 95 Hospital of China RongTong Medical and Health Group, Putian, Fujian, China.
Jianhui ChenDepartment of Critical Care Medicine, Affiliated Hospital of Putian University, Putian, Fujian, China.
Shijun ChenDepartment of Critical Care Medicine, Affiliated Hospital of Putian University, Putian, Fujian, China.
Jianhuang HuangDepartment of Neurosurgery, Affiliated Hospital of Putian University, Putian, Fujian, China.
Jianxiong HuDepartment of Critical Care Medicine, Affiliated Hospital of Putian University, Putian, Fujian, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Blood-brain barrier (BBB) disruption is a hallmark of acute traumatic brain injury (TBI), yet the immune-vascular mechanisms underlying endothelial dysfunction remain incompletely understood. Perivascular macrophages (PVMs) are strategically positioned to modulate cerebrovascular homeostasis, but their role in acute post-traumatic endothelial activation has not been systematically characterized. Methods: We re-analyzed a publicly available mouse single-cell RNA sequencing (scRNA-seq) dataset (GSE290150, 24 h post-TBI) to characterize the landscape of immune and vascular cell populations and to infer intercellular communication. Bone marrow-derived macrophages (BMDMs) served as a PVM surrogate model, and bEnd.3 cerebral endothelial cells were used for Results: Single-cell analysis revealed concurrent expansion of PVM-like cells and activated endothelial cells (Activated ECs) in the TBI brain, with CellChat-predicted enhancement of MIF-ACKR3 signaling from PVM-like cells toward Activated ECs. Inflammatory stimulation of BMDMs significantly increased MIF expression and secretion in a STAT3-dependent manner. Macrophage-conditioned medium induced endothelial activation-associated molecular changes, including upregulation of Angpt2 and Adm and downregulation of tight junction genes Claudin5 and Tjp1; these effects were attenuated by MIF inhibitor ISO-1 or ACKR3 antagonist CCX771. Recombinant MIF dose-dependently reproduced these changes, which were substantially abrogated by ACKR3 pharmacological blockade or siRNA knockdown. STAT3 inhibition further suppressed rMIF-induced endothelial transcriptional responses. Conclusion: These findings provide transcriptomic and

Indexed as

ACKR3blood–brain barrierendothelial activationMIFneurovascular unitperivascular macrophagestraumatic brain injury

Identifiers

PMID42682555
PMCPMC13529476

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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.