Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Friday, September 26, 2025

Exosomal miR-450b-5p Secreted from Exendin-4-Stimulated Endothelial Cells Protects Retinal Ganglion Cells Against Ischemia Reperfusion Injury

 Do you have 'professional' doctors who will ensure that this gets tested in stroke patients? NO? So, everyone in your stroke hospital is fucking incompetent?

Yeah, this is for retinal but can't anyone in stroke think outside the box and see if this is generalizable to all reperfusion injury?

Let's see how long your stroke hospital has been incompetent in NOT SOLVING reperfusion injury!
  • reperfusion injury (39 posts to January 2013)
  • ischemia-reperfusion injury (13 posts to October 2018)

    • Exosomal miR-450b-5p Secreted from Exendin-4-Stimulated Endothelial Cells Protects Retinal Ganglion Cells Against Ischemia Reperfusion Injury

    Authors Sun Y, Zhai R, Sheng Q, Ying Y, Kwan YL, Fan X, Xu H , Kong X

    Received 23 March 2025

    Accepted for publication 5 July 2025

    Published 25 September 2025 Volume 2025:20 Pages 11881—11894

    DOI https://doi.org/10.2147/IJN.S525339

    Checked for plagiarism Yes

    Review by Single anonymous peer review

    Peer reviewer comments 3

    Editor who approved publication: Dr Kamakhya Misra


    Yanan Sun,1,2,* Ruyi Zhai,1,* Qilian Sheng,1,* Yue Ying,1,* Ye Lin Kwan,1 Xintong Fan,1 Huan Xu,1 Xiangmei Kong11Eye Institute and Department of Ophthalmology, Eye & ENT Hospital, Fudan University, National Health Commission Key Laboratory of Myopia (Fudan University), Key Laboratory of Myopia, Chinese Academy of Medical Sciences, Shanghai Key Laboratory of Visual Impairment and Restoration, Shanghai, People’s Republic of China; 2Shenzhen Eye Hospital, Shenzhen Eye Medical Center, Southern Medical University, Shenzhen, People’s Republic of China *These authors contributed equally to this work Correspondence: Xiangmei Kong, Eye Institute and Department of Ophthalmology, Eye & ENT Hospital, Fudan University, 83 Fenyang Road, Xuhui District, Shanghai, 200031, People’s Republic of China, Tel +86 2164377134, Email kongxm95@163.com Huan Xu, Eye Institute and Department of Ophthalmology, Eye & ENT Hospital, Fudan University, 83 Fenyang Road, Xuhui District, Shanghai, 200031, People’s Republic of China, Tel +86 2164377134, Email xuhuan320@163.com

    Background: Retinal ischemia-reperfusion (RIR) injury represents a critical pathophysiological mechanism underlying various ocular ischemic diseases, characterized by progressive loss of retinal ganglion cells (RGCs). Exendin-4 (Ex-4), a widely used glucagon-like peptide-1 receptor (GLP-1R) agonist drug in the treatment of type 2 diabetes mellitus, has been reported to protect against ischemia-reperfusion (IR) injury in various vital organs. However, the potential neuroprotective effect of Ex-4 under RIR injury has been poorly understood.
    Methods: Immunofluorescence staining assay, hematoxylin and eosin (HE) staining were conducted to evaluate the neuroprotective role of Ex-4. A co-culture assay of human retinal vascular endothelial cells (HRVECs) and RGCs was established. Extracellular vesicles (EVs) were isolated from the culture supernatant of HRVECs with (E-EVs) or without Ex-4 treatment (O-EVs) under oxygen-glucose deprivation/reoxygenation (OGD/R) condition. Transmission electron microscopy (TEM), Nanoparticle tracking analysis (NTA) and Nano-flow cytometry (NanoFCM) were used to detect the presence and purity of EVs. Cell activity, reactive oxygen species (ROS) level, and cell death rate of RGCs were evaluated. Further global miRNA sequencing was performed on E-EVs or O-EVs to explore potential mechanisms.
    Results: Our findings revealed that Ex-4 had a GLP-1R-dependent neuroprotective effect on RGCs. Vascular endothelial cells (VECs) -derived EVs mediate the protective effect of Ex-4 on RGCs under acute RIR injury. We identified miR-450b-5p as a highly enriched miRNA in E-EVs. Treatment with either E-EVs or miR-450b-5p mimics significantly protected RGCs against RIR-induced injury. Mechanistic investigations identified acyl-coenzyme A (CoA) synthetase long-chain family member 4 (ACSL4) as a direct target of miR-450b-5p.
    Conclusion: Ex-4 exerts its neuroprotective effects under RIR injury by stimulating retinal VECs to secrete miR-450b-5p-enriched EVs, thereby revealing a novel endothelial-mediated neuroprotective pathway in ischemia diseases.

    Keywords: exendin-4, retinal ganglion cells, ischemia reperfusion injury, retinal vascular endothelial cells, extracellular vesicles, microRNA
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