OSCR

Mechanical pressure on endothelial cells mediates remote ischaemic preconditioning-induced neuroprotection via miR-126.

Overview

Authors: Xiaojie Wang1, Lei Yan1,2,3, Hongwei Zhu4, Yifan Li4, Qi Liu4, Wei Li1,2,3, Kerui Gong5, Zhijun Zhao6, Chunyang Zhang6, Gang Fu3, Guo Shao1,2,3,6, Xunming Ji1
ORCID iDs: Guo Shao
  1. Beijing Key Laboratory of Hypoxic Conditioning Translational Medicine, Xuanwu Hospital Capital Medical University, Beijing, PR China
  2. Inner Mongolia Key Laboratory of Hypoxic Translational Medicine, Baotou Medical college, Baotou, PR China
  3. Center for Translational Medicine, The Third People's Hospital of Longgang, Clinical Institute of Shantou University Medical college (The Third People's Hospital of Longgang District Shenzhen), Shenzhen, PR China
  4. Ultrasound Imaging Department, The Second Affiliated Hospital of Baotou Medical College, Baotou, PR China
  5. Department of Oral and Maxillofacial Surgery, University of California San Francisco, San Francisco, California, USA
  6. Department of Neurosurgery, The First Affiliated Hospital of Baotou Medical College, Baotou, PR China
Journal: Experimental physiology, article 10.1113/EP093541
Dates: received 4 December 2025; accepted 27 July 2026; published online 6 September 2026; in print September 2026
Type: Research article · Language: English
License: CC BY
Identifiers: DOI 10.1113/ep093541 · PMID 42702849 · PMCID PMC13547709 · OpenAlex W7211905121
Open access: gold, a free copy (OpenAlex)
Status: data only
Categories: human (organism), cellular / molecular (subfield)
Methods: Statistics, Smoothing, state filtering, decompositions
Keywords: endothelial cells, higher pressure, miR‐126, neuroprotection, remote ischaemic preconditioning
Topic: Cardiac Ischemia and Reperfusion (Pathology and Forensic Medicine, Medicine), according to OpenAlex
Funding: National Natural Science Foundation of China (81660307, 82060337)
Citations: cited by 1 paper (Europe PMC); 62 references in the paper

Abstract

Remote ischaemic preconditioning (RIPC) uses brief limb ischaemia to protect distant organs, but the mechanism of travel of the protective signal remains unclear. This study investigated whether endothelial cells (ECs) contribute to RIPC‐induced neuroprotection and the underlying mechanisms. Ten healthy volunteers (5 men, 5 women) underwent RIPC. Blood velocity was measured by Doppler ultrasound, and vascular wall pressure (VWP) was computed from 3D fluid‐structure interaction models based on magnetic resonance imaging data. Human microvascular endothelial cells (HMEC‐1) were exposed to cyclic higher pressure (CHP) for five cycles. miR‐126 expression and promoter DNA methylation were assessed by real‐time PCR and bisulfite sequencing. DNA methyltransferases (DNMTs) and global methylation levels were measured. SH‐SY5Y neurons were incubated with exosomes from HMEC‐1 culture medium and then subjected to oxygen–glucose deprivation/reperfusion (OGD/R). Neuronal viability and apoptosis were evaluated by MTS assay and flow cytometry, and damage by spectrin and cleaved caspase‐3 levels. Dicrotic waves were induced in 9 of the 10 participants following RIPC treatment. VWP transiently increased following RIPC. CHP reduced the expression and activity of DNMTs and induced the hypomethylation of the miR‐126 promoter sequence in HMEC‐1 cells, leading to an increase in miR‐126 levels. Exosomes from CHP‐treated HMEC‐1 cells decreased SH‐SY5Y cell injury under OGD/R. RIPC transiently increased VWP in healthy volunteers. The results of this study indicate that CHP treatment may induce the production of neuroprotective molecules by ECs, which may protect against ischaemia/hypoxia‐induced neuronal cell injury in vitro, possibly through a CHP‐induced effect involving miR‐126.

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

Data links

Data availability statement

The microRNA sequencing datasets generated and analysed during the current study are available in the NCBI Sequence Read Archive (SRA) repository, accession number PRJNA1302644(http://www.ncbi.nlm.nih.gov/bioproject/1302644.). Other data generated in the present study are included in the figures and/or tables of this article.

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, pages, dates, 12 authors, 5 keywords, 1 funder, 62 references.

Cite

This paper

Wang, X., Yan, L., Zhu, H., Li, Y., Liu, Q., Li, W., Gong, K., Zhao, Z., Zhang, C., Fu, G., Shao, G., & Ji, X. (2026). Mechanical pressure on endothelial cells mediates remote ischaemic preconditioning-induced neuroprotection via miR-126. Experimental physiology, 10.1113/EP093541. https://doi.org/10.1113/ep093541

BibTeX

@article{wang2026mechanical,
author = {Wang, Xiaojie and Yan, Lei and Zhu, Hongwei and Li, Yifan and Liu, Qi and Li, Wei and Gong, Kerui and Zhao, Zhijun and Zhang, Chunyang and Fu, Gang and Shao, Guo and Ji, Xunming},
title = {{Mechanical pressure on endothelial cells mediates remote ischaemic preconditioning-induced neuroprotection via miR-126}},
journal = {Experimental physiology},
year = {2026},
month = sep,
pages = {10.1113/EP093541},
publisher = {Wiley},
issn = {0958-0670},
doi = {10.1113/ep093541},
url = {https://doi.org/10.1113/ep093541},
pmid = {42702849},
pmcid = {PMC13547709}
}

RIS

TY - JOUR
AU - Wang, Xiaojie
AU - Yan, Lei
AU - Zhu, Hongwei
AU - Li, Yifan
AU - Liu, Qi
AU - Li, Wei
AU - Gong, Kerui
AU - Zhao, Zhijun
AU - Zhang, Chunyang
AU - Fu, Gang
AU - Shao, Guo
AU - Ji, Xunming
TI - Mechanical pressure on endothelial cells mediates remote ischaemic preconditioning-induced neuroprotection via miR-126
T2 - Experimental physiology
J2 - Exp Physiol
PY - 2026
DA - 2026/09/06
SP - 10.1113/EP093541
SN - 0958-0670
PB - Wiley
DO - 10.1113/ep093541
UR - https://doi.org/10.1113/ep093541
LA - en
ER -

CSL-JSON

{
"id": "10.1113/ep093541",
"type": "article-journal",
"title": "Mechanical pressure on endothelial cells mediates remote ischaemic preconditioning-induced neuroprotection via miR-126",
"container-title": "Experimental physiology",
"author": [
{
"family": "Wang",
"given": "Xiaojie"
},
{
"family": "Yan",
"given": "Lei"
},
{
"family": "Zhu",
"given": "Hongwei"
},
{
"family": "Li",
"given": "Yifan"
},
{
"family": "Liu",
"given": "Qi"
},
{
"family": "Li",
"given": "Wei"
},
{
"family": "Gong",
"given": "Kerui"
},
{
"family": "Zhao",
"given": "Zhijun"
},
{
"family": "Zhang",
"given": "Chunyang"
},
{
"family": "Fu",
"given": "Gang"
},
{
"family": "Shao",
"given": "Guo"
},
{
"family": "Ji",
"given": "Xunming"
}
],
"container-title-short": "Exp Physiol",
"page": "10.1113/EP093541",
"DOI": "10.1113/ep093541",
"PMID": "42702849",
"PMCID": "PMC13547709",
"ISSN": "0958-0670",
"publisher": "Wiley",
"URL": "https://doi.org/10.1113/ep093541",
"language": "en",
"issued": {
"date-parts": [
[
2026,
9,
6
]
]
}
}

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:10.3389/fimmu.2026.1745433
Integrative multi-omics analysis reveals inflammation-related molecular networks in acute mountain sickness.
Journal: Frontiers in immunology
In common: cellular / molecular, 2 references
[2] doi:10.1002/jev2.70311
Status Epilepticus Alters the Function of Brain-Derived Extracellular Vesicles.
Journal: Journal of extracellular vesicles
In common: cellular / molecular, 1 reference
[3] doi:10.3389/fphys.2026.1781613
Transcriptomic analysis and experimental verification reveal the involvement of PI3K/AKT signaling pathway in high-altitude cognitive dysfunction.
Journal: Frontiers in physiology
In common: cellular / molecular, 1 reference
[4] doi:10.1038/s44385-026-00090-w
Focused ultrasound-induced cavitation in a human brain microphysiological system produces injury signaling biomarkers consistent with blast trauma.
Journal: npj biomedical innovations
In common: 1 reference
[5] doi:10.1371/journal.ppat.1014603
Analysis of host and viral nascent and steady-state RNA levels in a human neuronal model of herpes simplex virus 1 infection.
Journal: PLoS pathogens
In common: cellular / molecular, 1 reference
[6] doi:10.1155/humu/4225263
The Charcot-Marie-Tooth Neuropathy (CMTX3) Complex Structural Variation Causes Differential SOX3 Spatiotemporal Expression.
Journal: Human mutation
In common: cellular / molecular, 1 reference
[7] doi:10.1186/s12974-026-03970-5
Estrogen deprivation exacerbates Alzheimer's disease pathology through neuronal CTSS signaling.
Journal: Journal of neuroinflammation
In common: cellular / molecular, 1 reference
[8] doi:10.1126/sciadv.aed2952 [code]
Activation of transposable elements is linked to a region- and cell type-specific interferon response in Parkinson's disease.
Journal: Science advances
In common: cellular / molecular, 1 reference
[9] doi:10.1002/alz.71804
A meta-refined human Alzheimer's disease-associated gene subset shows partial mouse-model pathway correspondence and limited cross-cohort machine-learning transportability.
Journal: Alzheimer's & dementia : the journal of the Alzheimer's Association
In common: cellular / molecular, 1 reference
[10] doi:10.1101/gr.280394.124 [code]
De novo structural variants in autism spectrum disorder disrupt distal regulatory interactions of neuronal genes.
Journal: Genome research
In common: 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.

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.