Exosomal miR-199a-5p derived from endothelial cells attenuates apoptosis and inflammation in neural cells by inhibiting endoplasmic reticulum stress

Yu, Yunhu; Zhou, Hang; Xiong, Yanquan; Liu, Jigang

doi:10.1016/j.brainres.2019.146515

Cited by 30 publications

(18 citation statements)

References 14 publications

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“…numerous studies have proved that er stress contributed to apoptotic activity following cerebral i/r injury (6,(32)(33)(34)(35). These effects appeared to be partially mediated by the upregulation of er stress markers, including cHoP, eukaryotic initiation factor 2α and GrP78 (6,32).…”

Section: Discussionmentioning

confidence: 99%

“…These effects appeared to be partially mediated by the upregulation of er stress markers, including cHoP, eukaryotic initiation factor 2α and GrP78 (6,32). Previous work has demonstrated that er stress exerted a positive effect on neuronal apoptosis and the detection of cellular damage in ischemic stroke (33,34). GrP78 is an er resident protein triggered by microenvironmental damage that disturbs er function (35).…”

Section: Discussionmentioning

confidence: 99%

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Astragalin alleviates ischemia/reperfusion‑induced brain injury via suppression of endoplasmic reticulum stress

Liu

Wang

et al. 2020

Mol Med Rep

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excessive apoptosis and neuronal dysfunction are pathological features of ischemic stroke. Previous studies have demonstrated that astragalin (aST) exerted both antiapoptotic and anti-inflammatory effects in several types of disease, although its potential effect in ischemic stroke remains unclear. The purpose of the present study was to investigate the effects of aST on cerebral ischemia/reperfusion (i/r)-induced brain injury and the underlying mechanisms. Brain injury was assessed in an experimental rat model using measurement of neurological scores and inflammatory factors. To assess the role of aST in i/r-induced brain injury and the potential mechanism of action, SH5Y were treated with thapsigargin and aST. apoptotic rate and er stress levels were measured by western blotting, reverse transcription-quantitative PCR and immunofluorescence staining. It was discovered that AST significantly improved long-term neurological outcomes in rats following cerebral i/r injury, through the attenuation of the expression levels of apoptotic proteins (Bax and cleaved-caspase-3) and the release of inflammatory cytokines, as well as upregulating the expression levels of the anti-apoptotic protein Bcl-2. Furthermore, aST attenuated the expression levels of the endoplasmic reticulum (er) stress-related protein, glucose-regulated protein, 78 kda, as well as its downstream apoptotic mediators (cHoP and caspase-12). Thapsigargin-induced er stress activation and apoptosis were also attenuated by aST in an in vitro neuronal cell culture model. in conclusion, these results suggested that aST may protect against i/r-induced brain injury, thus, highlighting its therapeutic potential in patients with ischemic stroke.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Astragalin alleviates ischemia/reperfusion‑induced brain injury via suppression of endoplasmic reticulum stress

Liu

Wang

et al. 2020

Mol Med Rep

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“…The anti-apoptotic effect of HUVECs-exos was in consistent with previous results. Evidence has shown that HUVECsexos could induce anti-apoptotic influence on neural cells (41,42). Inhibition of miR-21-3p's binding target ATG12 regulated the apoptotic pathway by suppressing autophagy or inactivating Bcl-2 family members (42).…”

Section: Discussionmentioning

confidence: 99%

Exosome-derived miR-196b-5p facilitates intercellular interaction in infantile hemangioma via down-regulating CDKN1B

Wang¹,

Zhao²,

Liu³

et al. 2021

Ann Transl Med

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Background: Though infantile hemangioma (IH) is a common benign vascular tumor, its pathogenesis remains unclear. This study explored the function of hemangioma-derived stem cells (HemSCs) derived exosomes, which exerted an intercellular effect on hemangioma-derived endothelial cells (HemECs).Methods: First, HemSCs and HemECs were extracted and cultured. HemSCs derived exosomes (HemSCsexos) were harvested. miRNA sequencing and target prediction were used to explore differentially expressed miRNAs and potential binding targets. After HemECs were co-cultured with HemSCs-exos, a series of in vitro assays were then performed including cell counting kit-8 (CCK-8) assay, cell apoptosis assay, cell cycle assay and tube formation assay to evaluate proliferation, angiogenesis abilities, etc. qRT-PCR and Western blot were conducted to detect the expression level of target genes and proteins.Results: After co-culturing with HemSCs-exos, proliferation, and angiogenesis abilities of HemECs were enhanced, while apoptosis and cell cycle arrest rate were decreased. MiR-196b-5p was observed to be significantly highly expressed in HemSCs-exos. CDKN1B was identified as the binding target of miR-196b-5p. HemECs' proliferation and angiogenesis abilities were elevated when co-cultured with exosomes from HemSCs transfected with miR-196b-5p mimic. In addition, apoptosis rate declined, and lower cells were arrested in G0/G1 phases. Cyclin E, bcl-2 were significantly highly expressed, whereas p27, Bax expression were significantly down-regulated. The positive effect of miR-196b-5p in HemSCs-exos was dramatically reversed when HemECs were transfected with oe-CDKN1B. Conclusions:The current study found a novel intercellular interaction between IH cells. Briefly, exosomederived miRNA-196b-5p in HemSCs could facilitate proliferation and angiogenesis abilities, and attenuate apoptosis and cell cycle repression rate of HemECs by directly binding with CDKN1B.

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“…The exosomes that were found to contain miR-199a lowered endoplasmic reticulum stress, protecting neural cells from the potential effects of the stress. This seems to show that secretion of exosomes from immune or nonimmune cells may reduce inflammation while simultaneously promoting tissue repair/regeneration [115]. Borges et al showed that tubular epithelial cells of mouse kidneys produced hypoxia-evoked exosomes that led to the activation of tissue fibroblasts, resulting in regeneration and fibrosis.…”

Section: Exosomes As Immunosuppressive Mediating Variables In Chronic Inflammatory Microenvironmentsmentioning

confidence: 99%

Extracellular Vesicles (Exosomes) as Immunosuppressive Mediating Variables in Tumor and Chronic Inflammatory Microenvironments

Awadasseid

Zhang

2021

Cells

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Exosomes are extracellular vesicles released by most of the eukaryotic cells. Exosomes’ components include proteins, lipids, microRNA, circular RNA, long noncoding RNA, DNA, etc. Exosomes may carry both pro and anti-inflammatory cargos; however, exosomes are predominantly filled with immunosuppressive cargos such as enzymes and microRNAs in chronic inflammation. Exosomes have surfaced as essential participants in physiological and pathological intercellular communication. Exosomes may prevent or promote the formation of an aggressive tumor and chronic inflammatory microenvironments, thus influencing tumor and chronic inflammatory progression as well as clinical prognosis. Exosomes, which transmit many signals that may either enhance or constrain immunosuppression of lymphoid and myeloid cell populations in tumors, are increasingly becoming recognized as significant mediators of immune regulation in cancer. In this review, we outline the function of exosomes as mediators of immunosuppression in tumor and chronic inflammatory microenvironments, with the aim to improve cancer therapy.

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Exosomal miR-199a-5p derived from endothelial cells attenuates apoptosis and inflammation in neural cells by inhibiting endoplasmic reticulum stress

Cited by 30 publications

References 14 publications

Astragalin alleviates ischemia/reperfusion‑induced brain injury via suppression of endoplasmic reticulum stress

Astragalin alleviates ischemia/reperfusion‑induced brain injury via suppression of endoplasmic reticulum stress

Exosome-derived miR-196b-5p facilitates intercellular interaction in infantile hemangioma via down-regulating CDKN1B

Extracellular Vesicles (Exosomes) as Immunosuppressive Mediating Variables in Tumor and Chronic Inflammatory Microenvironments

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