ArticleBrain hemorrhages2021
Therapeutic effects of exosomes from angiotensin-converting enzyme 2 - overexpressed endothelial progenitor cells on intracerebral hemorrhagic stroke.
Article in Brain hemorrhages, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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.
The trial behind it
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Who cites it
3 citing papers in PubMed.
- Novel Therapeutic Mechanisms and Strategies for Intracerebral Hemorrhage: Focusing on Exosomes.International journal of nanomedicine · 2024Review
- Engineered Extracellular Vesicles for Drug Delivery in Therapy of Stroke.Pharmaceutics · 2023Review
- Cardioprotective Roles of Endothelial Progenitor Cell-Derived Exosomes.Frontiers in cardiovascular medicine · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Objective: We have previously demonstrated that angiotensin-converting enzyme 2 (ACE2) could boost the therapeutic effects of endothelial progenitor cells (ACE2-EPCs) on stroke. However, where this effect comes from is still unclear. Here, we investigated whether the exosomes (EXs) released from ACE2-EPCs could provide the benefit for acute intracerebral hemorrhagic stroke (ICH). Methods: The C57BL/6 mice were induced ICH by collagenase injection, followed by intravenously administration of ACE2-EPC-EXs. ACE2 blocker, DX600 was used to verify the effects of ACE2. The neurological deficit score (NDS), hemorrhage volume, brain water content, and blood-brain barrier (BBB) permeability were measured at day 2 after injection. The levels of ACE2 and inflammatory factors/genes in the brain were also measured. Results: EPC-EXs decreased hemorrhage volume, brain edema, BBB permeability, and improved NDS, which were enhanced by ACE2-EPC-EXs treatment; 2) As compared to EPC-EXs, ACE2-EPC-EXs resulted in an up-regulation of ACE2 in the brain, associating with the down-regulated expressions of TNF-α and NFκB and up-regulated level of IκBα. 3) DX600 blocked the above mentioned protective effects of ACE2-EPC-EXs in ICH mice. Conclusion: These data suggest that the infusion of ACE2-EPC-EXs could provide the therapeutic effect on acute ICH by alleviating the post-stroke inflammation via transferring ACE2.
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