Correction to: Human embryonic stem cell-derived extracellular vesicles alleviate retinal degeneration by upregulating Oct4 to promote retinal Müller cell retrodifferentiation via HSP90

Ke, Yifeng; Fan, Xiaoe; Hao, Rui; Dong, Lijie; Xue, Min; Tan, Liangzhang; Yang, Chunbo; Li, Xiaorong; Ren, Xinjun

doi:10.1186/s13287-021-02213-z

Cited by 3 publications

(2 citation statements)

References 1 publication

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“…It is well known that HSP90 is secreted from cells by exosomes [ 12 ]. HSP90 in human embryonic stem cell-derived extracellular vesicles (exosomes) was shown to alleviate retinal degeneration by promoting retinal Müller cell retrodifferentiation [ 39 ]. Although increasing evidence suggests that HSP90 participates in cardioprotection against I/R, no study has addressed the function of HSP90 in exosomes induced by RIPC.…”

Section: Discussionmentioning

confidence: 99%

Exosomal HSP90 induced by remote ischemic preconditioning alleviates myocardial ischemia/reperfusion injury by inhibiting complement activation and inflammation

Cheng

Zhong

et al. 2023

BMC Cardiovasc Disord

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Background/Aims The activation of the complement system and subsequent inflammatory responses are important features of myocardial ischemia/reperfusion (I/R) injury. Exosomes are nanoscale extracellular vesicles that play a significant role in remote ischemic preconditioning (RIPC) cardioprotection. The present study aimed to test whether RIPC-induced plasma exosomes (RIPC-Exo) exert protective effects on myocardial I/R injury by inhibiting complement activation and inflammation and whether exosomal heat shock protein 90 (HSP90) mediates these effects. Methods Rat hearts underwent 30 min of coronary ligation followed by 2 h of reperfusion. Plasma exosomes were isolated from RIPC rats and injected into the infarcted myocardium immediately after ligation. Sixty rats were randomly divided into Sham, I/R, I/R + RIPC-Exo (50 µg/µl), and RIPC-Exo + GA (geldanamycin, 1 mg/kg, administration 30 min before ligation) groups. Cardiomyocyte apoptosis, the release of myocardial markers (LDH, cTnI and CK-MB), infarct size, the expression of HSP90, complement component (C)3, C5a, c-Jun N-terminal kinase (JNK), interleukin (IL)-1β, tumor necrosis factor (TNF)-alpha and intercellular adhesion molecule -1 (ICAM-1) were assessed. Results RIPC-Exo treatment significantly reduced I/R-induced cardiomyocyte apoptosis, the release of myocardial markers (LDH, cTnI and CK-MB) and infarct size. These beneficial effects were accompanied by decreased C3 and C5a expression, decreased inflammatory factor levels (IL-1β, TNF-α, and ICAM-1), decreased JNK and Bax, and increased Bcl-2 expression. Meanwhile, the expression of HSP90 in the exosomes from rat plasma increased significantly after RIPC. However, treatment with HSP90 inhibitor GA significantly reversed the cardioprotection of RIPC-Exo, as well as activated complement component, JNK signalling and inflammation, indicating that HSP90 in exosomes isolated from the RIPC was important in mediating the cardioprotective effects during I/R. Conclusion Exosomal HSP90 induced by RIPC played a significant role in cardioprotection against I/R injury, and its function was in part linked to the inhibition of the complement system, JNK signalling and local and systemic inflammation, ultimately alleviating I/R-induced myocardial injury and apoptosis by the upregulation of Bcl-2 expression and the downregulation of proapoptotic Bax.

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Section: Discussionmentioning

confidence: 99%

Exosomal HSP90 induced by remote ischemic preconditioning alleviates myocardial ischemia/reperfusion injury by inhibiting complement activation and inflammation

Cheng

Zhong

et al. 2023

BMC Cardiovasc Disord

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show abstract

“…Exosomes derived from hESCs (hESCs-exo) carry hESC-specific miRNAs, mRNAs, and proteins, offering the regenerative potential of hESCs while avoiding their immune and ethical problems [24]. Therefore, hESCs-exo have emerged as critical mediators in providing an alternate cell-free therapeutic modality [25][26][27]. Several studies have shown that exosomes from embryonic stem cells can reduce inflammation and pyroptosis, such as increasing the expressions of the anti-inflammatory cytokines IL-10, IL-4, IL-9, and IL-13 [28,29] and reducing pyroptosis in doxorubicin-induced cardiomyopathy [29].…”

Section: Introductionmentioning

confidence: 99%

Human Embryonic Stem-Cell-Derived Exosomes Repress NLRP3 Inflammasome to Alleviate Pyroptosis in Nucleus Pulposus Cells by Transmitting miR-302c

Xian

et al. 2023

IJMS

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Recent studies have shown that the NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3) inflammasome is extensively activated in the process of intervertebral disc degeneration (IVDD), leading to the pyroptosis of nucleus pulposus cells (NPCs) and the exacerbation of the pathological development of the intervertebral disc (IVD). Exosomes derived from human embryonic stem cells (hESCs-exo) have shown great therapeutic potential in degenerative diseases. We hypothesized that hESCs-exo could alleviate IVDD by downregulating NLRP3. We measured the NLRP3 protein levels in different grades of IVDD and the effect of hESCs-exo on the H2O2-induced pyroptosis of NPCs. Our results indicate that the expression of NLRP3 was upregulated with the increase in IVD degeneration. hESCs-exo were able to reduce the H2O2-mediated pyroptosis of NPCs by downregulating the expression levels of NLRP3 inflammasome-related genes. Bioinformatics software predicted that miR-302c, an embryonic stem-cell-specific RNA, can inhibit NLRP3, thereby alleviating the pyroptosis of NPCs, and this was further verified by the overexpression of miR-302c in NPCs. In vivo experiments confirmed the above results in a rat caudal IVDD model. Our study demonstrates that hESCs-exo could inhibit excessive NPC pyroptosis by downregulating the NLRP3 inflammasome during IVDD, and miR-302c may play a key role in this process.

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Towards Stem/Progenitor Cell-Based Therapies for Retinal Degeneration

Liu,

Lu,

Chen

et al. 2024

Stem Cell Rev and Rep

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Correction to: Human embryonic stem cell-derived extracellular vesicles alleviate retinal degeneration by upregulating Oct4 to promote retinal Müller cell retrodifferentiation via HSP90

Abstract: An amendment to this paper has been published and can be accessed via the original article.

Cited by 3 publications

References 1 publication

Exosomal HSP90 induced by remote ischemic preconditioning alleviates myocardial ischemia/reperfusion injury by inhibiting complement activation and inflammation

Exosomal HSP90 induced by remote ischemic preconditioning alleviates myocardial ischemia/reperfusion injury by inhibiting complement activation and inflammation

Human Embryonic Stem-Cell-Derived Exosomes Repress NLRP3 Inflammasome to Alleviate Pyroptosis in Nucleus Pulposus Cells by Transmitting miR-302c

Towards Stem/Progenitor Cell-Based Therapies for Retinal Degeneration

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