OSCR

Polymersomes preventing brain infiltration of CD177<sup>+</sup> neutrophils to mitigate hemorrhagic transformation post-tPA thrombolysis.

Overview

Authors: Zhenhua Wang1, Hua Liu2, Zhiyao Xu2, Cheng Huang1, Xing Guo1, Shaobing Zhou1
  1. Institute of Biomedical Engineering, College of Medicine, Southwest Jiaotong University,Chengdu, PR China
  2. Department of Neurology, The Third People’s Hospital of Chengdu,Chengdu, PR China
Journal: Nature communications, volume 17, issue 1, article 4395
Dates: received 5 June 2025; accepted 12 March 2026; published online 25 March 2026
Type: Research article · Language: English
License: CC BY
Identifiers: DOI 10.1038/s41467-026-71076-w · PMID 41881994 · PMCID PMC13181025 · OpenAlex W7140285352
Open access: gold, a free copy (OpenAlex)
Categories: human (organism), mouse (organism), stroke (population)
Methods: Statistics, Smoothing, state filtering, decompositions, Machine learning
Keywords: Drug delivery, Coagulation system
MeSH: Fibrinolytic Agents*, Hemorrhagic Stroke*, Neutrophils*, Thrombolytic Therapy*, Tissue Plasminogen Activator*, Animals, Brain, Cell Line, Cerebral Hemorrhage, GPI-Linked Proteins, Humans, Isoantigens, Male, Mice, Mice, Inbred C57BL, Polymers, Reactive Oxygen Species, Receptors, Cell Surface, Recombinant Proteins (* major topic)
Topic: Neutrophil, Myeloperoxidase and Oxidative Mechanisms (Immunology, Immunology and Microbiology), according to OpenAlex
Funding: National Natural Science Foundation of China (U22A20161, 52495011, 52473324)
Citations: not cited yet (Europe PMC); 75 references in the paper

Abstract

As an intravenous thrombolytic agent, tissue plasminogen activator (tPA) is limited by hemorrhagic transformation (HT) and a narrow therapeutic time window. Here we develop ROS-triggered polymersomes conjugated with fibrin-targeting CREKA peptide (CP) for tPA encapsulation. achieves efficient thrombosis targeting and enhanced thrombolytic efficacy, however, it has not been able to avert the occurrence of hemorrhage subsequent to thrombolysis. Building from our clinical discovery that stroke patients suffer from tPA-induced HT featured strong expression of CD177, recombinant CD177 protein (rCD177) was loaded into CP polymersomes as nanomedicine and administrated prior to thrombolysis. rCD177 can be released in response to elevated ROS within the obstructed vessels, which binds to endothelial cells through interacting with CD31 and efficiently prevents the migration of CD177+ neutrophils into the brain parenchyma. The reduced CD177+ neutrophils suppress the generation of neutrophil extracellular traps (NETs), thereby dampening the inflammatory activation of microglia and ultimately improving the prognosis of HT. This innovative strategy presents a promising avenue for attenuating hemorrhagic complications post-thrombolysis

Reproduced under the paper's license (CC BY), from the paper cited above.

Code

The paper links to its data and to no code of its authors: see the Data section.

The paper's code and data availability statement is in 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

Data availability

All data supporting the results of this study are included in the article and Supplementary Information. The RNA-seq has been deposited to NCBI under accession codes (PRJNA1331951 (https://www.ncbi.nlm.nih.gov/bioproject/PRJNA1331951), PRJNA1332825 (https://www.ncbi.nlm.nih.gov/bioproject/?term=PRJNA1332825)). Source data are provided with this paper.

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, 30 September 2026: the first record

Recorded: type, language, journal, volume, issue, pages, dates, 6 authors, 2 keywords, 19 MeSH terms, 1 funder, 74 references.

Cite

This paper

Wang, Z., Liu, H., Xu, Z., Huang, C., Guo, X., & Zhou, S. (2026). Polymersomes preventing brain infiltration of CD177<sup>+</sup> neutrophils to mitigate hemorrhagic transformation post-tPA thrombolysis. Nature communications, 17(1), 4395. https://doi.org/10.1038/s41467-026-71076-w

BibTeX

@article{wang2026polymersomes,
author = {Wang, Zhenhua and Liu, Hua and Xu, Zhiyao and Huang, Cheng and Guo, Xing and Zhou, Shaobing},
title = {{Polymersomes preventing brain infiltration of CD177\<sup\>+\</sup\> neutrophils to mitigate hemorrhagic transformation post-tPA thrombolysis}},
journal = {Nature communications},
year = {2026},
month = mar,
volume = {17},
number = {1},
pages = {4395},
publisher = {Nature Publishing Group},
issn = {2041-1723},
doi = {10.1038/s41467-026-71076-w},
url = {https://doi.org/10.1038/s41467-026-71076-w},
pmid = {41881994},
pmcid = {PMC13181025}
}

RIS

TY - JOUR
AU - Wang, Zhenhua
AU - Liu, Hua
AU - Xu, Zhiyao
AU - Huang, Cheng
AU - Guo, Xing
AU - Zhou, Shaobing
TI - Polymersomes preventing brain infiltration of CD177<sup>+</sup> neutrophils to mitigate hemorrhagic transformation post-tPA thrombolysis
T2 - Nature communications
J2 - Nat Commun
PY - 2026
DA - 2026/03/25
VL - 17
IS - 1
SP - 4395
SN - 2041-1723
PB - Nature Publishing Group
DO - 10.1038/s41467-026-71076-w
UR - https://doi.org/10.1038/s41467-026-71076-w
LA - en
ER -

CSL-JSON

{
"id": "10.1038/s41467-026-71076-w",
"type": "article-journal",
"title": "Polymersomes preventing brain infiltration of CD177<sup>+</sup> neutrophils to mitigate hemorrhagic transformation post-tPA thrombolysis",
"container-title": "Nature communications",
"author": [
{
"family": "Wang",
"given": "Zhenhua"
},
{
"family": "Liu",
"given": "Hua"
},
{
"family": "Xu",
"given": "Zhiyao"
},
{
"family": "Huang",
"given": "Cheng"
},
{
"family": "Guo",
"given": "Xing"
},
{
"family": "Zhou",
"given": "Shaobing"
}
],
"container-title-short": "Nat Commun",
"volume": "17",
"issue": "1",
"page": "4395",
"DOI": "10.1038/s41467-026-71076-w",
"PMID": "41881994",
"PMCID": "PMC13181025",
"ISSN": "2041-1723",
"publisher": "Nature Publishing Group",
"URL": "https://doi.org/10.1038/s41467-026-71076-w",
"language": "en",
"issued": {
"date-parts": [
[
2026,
3,
25
]
]
}
}

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/s41467-025-64518-4
An eNOS-like nanomaterial for specific reversal of cerebral ischemia-reperfusion injury.
Journal: Nature communications
In common: stroke, mouse, 3 references
[2] doi:10.1186/s12964-023-01379-8
Neutrophil extracellular traps mediated by platelet microvesicles promote thrombosis and brain injury in acute ischemic stroke.
Journal: Cell communication and signaling : CCS
In common: stroke, mouse, 3 references
[3] doi:10.1038/s44321-024-00117-y
Histidine-rich glycoprotein modulates neutrophils and thrombolysis-associated hemorrhagic transformation.
Journal: EMBO molecular medicine
In common: stroke, mouse, 3 references
[4] doi:10.1016/j.xcrm.2026.102640
Hierarchically collapsible nanoactuator modulates mitochondrial ferroptosis-bioenergetic homeostasis cascade to decouple ischemic stroke.
Journal: Cell reports. Medicine
In common: stroke, mouse, 3 references
[5] doi:10.1186/s12929-023-00954-y
Brain alarm by self-extracellular nucleic acids: from neuroinflammation to neurodegeneration.
Journal: Journal of biomedical science
In common: stroke, 3 references
[6] doi:10.1038/s41423-025-01363-x
FOXO1-driven metabolic reprogramming of hematomal CD8<sup>+</sup> T cells drives the expansion of perihematomal edema following intracerebral hemorrhage.
Journal: Cellular & molecular immunology
In common: stroke, mouse, 2 references
[7] doi:10.1002/advs.202503722
Neutrophil Mobilization Triggers Microglial Functional Change to Exacerbate Cerebral Ischemia-Reperfusion Injury.
Journal: Advanced science (Weinheim, Baden-Wurttemberg, Germany)
In common: stroke, mouse, 2 references
[8] doi:10.1007/s10565-024-09869-2
SIRT1 restores mitochondrial structure and function in rats by activating SIRT3 after cerebral ischemia/reperfusion injury.
Journal: Cell biology and toxicology
In common: stroke, 2 references
[9] doi:10.18632/aging.205415
Novel diagnostic biomarkers of oxidative stress, ferroptosis, immune infiltration characteristics and experimental validation in ischemic stroke.
Journal: Aging
In common: stroke, 2 references
[10] doi:10.1002/wsbm.1597
The role of STING signaling in central nervous system infection and neuroinflammatory disease.
Journal: WIREs mechanisms of disease
In common: stroke, 2 references

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: code errors and mismatches between the code and the paper about this paper and its code, from readers and its authors, beside the paper and its tracing map.

Reproductions: reports from readers who ran the authors' code and did not get the paper's result, what they ran, with which environment, commit and data.

Activity: what happens around this paper: new versions of its record, its map's validation, discussions and reproductions. It opens with sign-in.