&lt;p&gt;Bone marrow mesenchymal stem cell-derived exosomes attenuate D-GaIN/LPS-induced hepatocyte apoptosis by activating autophagy in vitro&lt;/p&gt;

Zhao, Shuxian; Liu, Yan; Pu, Zenghui

doi:10.2147/dddt.s220190

Cited by 75 publications

(54 citation statements)

References 46 publications

(38 reference statements)

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“…There were reports that exosomes could attenuate diabetic nephropathy and D-GaIN/LPS-induced hepatocyte injury by promoting autophagic ux and inhibiting apoptosis [31,32]. Therefore, we also examined whether exosomes could inhibit NPCs apoptosis by promoting autophagic ux.…”

Section: Resultsmentioning

confidence: 95%

Exosomes from normal cartilage endplate stem cells ameliorate intervertebral disc degeneration more effectively than exosomes from degenerated cartilage endplate stem cell by activating the AKT/autophagy pathway

Luo

Jian

Sun³

et al. 2020

Preprint

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Background Nucleus pulposus cells (NPCs) apoptosis is an important factor in exacerbating intervertebral disc degeneration (IVDD) that can be effectively suppressed by exosomes. The aim of this study was to reaearch whether normal cartilage endplate stem cells (CESCs) derived exosomes (N-Exos) were more conducive to activation of autophagy and inhibition of NPCs apoptosis and IVDD than degenerated CESCs derived exosomes (D-Exos) or not. Methods Rat CESCs were isolated and identified, and the exosomes produced by normal CESCs and degenerated CESCs were extracted. The bioinformatics differences between normal CESCs derived exosomes (N-Exos) and degenerated CESCs derived exosome (D-Exos) were analyzed by mass spectrometry, heat map and KEGG enrichment analysis biology. The effects of N-Exos and D-Exos on the inhibition of NPCs apoptosis were examined by TUNEL staining, flow cytometry and western blotting. The involvement of the AKT and autophagy signaling pathways was investigated using the signaling inhibitor LY294002. Magnetic resonance imaging, western blotting and immunofluorescence staining were used to evaluate the therapeutic effects of N-Exos in vivo. Results CESCs in the cartilage endplate (CEP) could secrete a large amount of exosomes. N-Exos were more conducive to activation of autophagy than D-Exos. The apoptotic rate of NPCs was decreased obviously after treatment with N-Exos than after D-Exos treatment. N-Exos inhibited NPCs apoptosis or attenuated IVDD in a rat tail model by activating the AKT and autophagy signaling pathways. Conclusions It was the first to confirm that CEP could delay the progression of IVDD through exosomes secreted by normal CESCs. The therapeutic effects of N-Exos on inhibiting NPCs apoptosis and slowing IVDD progression was more effective than D-Exos by activating the PI3K/AKT/autophagy pathway, which explained the reason that the incidence of IVDD was increased after inflammation of the CEP.

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Section: Resultsmentioning

confidence: 95%

Exosomes from normal cartilage endplate stem cells ameliorate intervertebral disc degeneration more effectively than exosomes from degenerated cartilage endplate stem cell by activating the AKT/autophagy pathway

Luo

Jian

Sun³

et al. 2020

Preprint

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“…In another hepatic injury study, the EVs from MSC exhibited protective effects on the hepatocytes despite being treated with liver injury stimulant drugs, partly via the upregulation of hepatocyte proliferation [74]. Other studies of EVs from the various origins of MSCs showed similar hepatic protective and regenerative effects, as seen in the bone-marrow-derived MSCs [75][76][77][78][79][80], human umbilical cord-derived MSCs [81][82][83], human liver stem cells [84,85], induced pluripotent stem cell-derived MSCs [86], human embryonic-derived MSCs [64], human menstrual blood-derived MSCs [87], and adipose-derived MSCs [88][89][90][91]. As for the prevention of fibrosis via the suppression of HSCs, a study of EVs from the chorionic plate-derived MSCs showed that these EVs suppressed the activation and proliferation of HSCs due to the presence of miR-125b in the cargo, thus preventing liver fibrosis [92].…”

Section: Evs From the Mesenchymal Stem Cells As A Treatment Optionmentioning

confidence: 82%

Extracellular Vesicles in the Development of the Non-Alcoholic Fatty Liver Disease: An Update

et al. 2020

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Non-alcoholic fatty liver disease (NAFLD) is a broad spectrum of liver damage disease from a simple fatty liver (steatosis) to more severe liver conditions such as non-alcoholic steatohepatitis (NASH), fibrosis, and cirrhosis. Extracellular vesicles (EVs) are a heterogeneous group of small membrane vesicles released by various cells in normal or diseased conditions. The EVs carry bioactive components in their cargos and can mediate the metabolic changes in recipient cells. In the context of NAFLD, EVs derived from adipocytes are implicated in the development of whole-body insulin resistance (IR), the hepatic IR, and fatty liver (steatosis). Excessive fatty acid accumulation is toxic to the hepatocytes, and this lipotoxicity can induce the release of EVs (hepatocyte-EVs), which can mediate the progression of fibrosis via the activation of nearby macrophages and hepatic stellate cells (HSCs). In this review, we summarized the recent findings of adipocyte- and hepatocyte-EVs on NAFLD disease development and progression. We also discussed previous studies on mesenchymal stem cell (MSC) EVs that have garnered attention due to their effects on preventing liver fibrosis and increasing liver regeneration and proliferation.

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“…Thus, at least, these pathways mediated autophagy flux inside cells [109]. Surprisingly, exosomal miR-30a and miR-125b-5p which derived from transplanted MSCs represents the protective effect on I/R-induced injuries in cardiomyocytes by autophagy regulation through the Akt/AMPK/mTOR pathways both in vitro and in vivo studies [116][117][118]. It seems that activation of the PI3K/AKT/mTOR signaling pathway reduces excessive autophagy and rescues cells from death.…”

Section: Cross-regulation By Akt/mtor Signaling Pathwaymentioning

confidence: 99%

“…Liu et al found that exosomes from MSCs increased autophagy in cardiomyocytes through AMPK/mTOR pathway and reduced adverse effects of myocardial I/R injury [109]. Besides, MSCs-derived exosomes transfer miR-30a and miR-125b-5p, which participate in improving I/R-induced injuries in cardiomyocytes by modulating autophagy via the Akt/mTOR signaling pathways both in vitro and in vivo studies [116][117][118]. Therefore, MSCs derived exosomes have potential to modulate autophagy in cells of cardiovascular system, proposing clinical application in CVD treatment.…”

Section: Clinical Translation Potential Of Exosomes-mediated Autophagymentioning

confidence: 99%

Exosomal cargos modulate autophagy in recipient cells via different signaling pathways

et al. 2020

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Vesicular system of mammalian cells is composed of two intracellular and extracellular vesicles systems, which contributes to the intra/intercellular communication and cellular homeostasis. These systems mediate transferring of biological molecules like proteins, nucleic acids, and lipids inside the cytoplasm, and between the cells. By the present study, authors describe molecular crosslink between exosome biogenesis and autophagy and take a certain focus on the autophagic cargos of exosomes and signaling pathways involved in exosome-induced autophagy in target cells and vice versa. Autophagy the generation of double-phospholipid vesicles, is a process that engulfs damaged proteins and organelles, share molecular similarity and function synergy with exosomes biogenesis for degradation or exocytosis of certain cargo. Exosomes, the smallest subtype of extracellular vesicles, originating from the membrane of the multivesicular body located inside cells demonstrate key roles in the intracellular and intercellular communication. Growing evidence demonstrates the interaction between exosome biogenesis and autophagy both at intertwined molecular pathways and crossbred vesicles known as amphisomes. Crosstalk between exosome biogenesis and autophagy contributes to maintain cellular homeostasis under external and internal stresses. Moreover, these processes can modulate each other via different signaling pathways. Exosomes contain autophagic cargos that induce autophagy via the cascade of molecular events in target cells, which called here exosome-induced autophagy. Taken together, crosstalk between exosome biogenesis and autophagy plays pivotal roles in cell homeostasis. Shedding light on the interaction between endomembrane systems may promote our knowledge about the relation between exosome and autophagy pathways in lysosome-related disorders against treatments; proposing a theoretical approach for therapy.

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<p>Bone marrow mesenchymal stem cell-derived exosomes attenuate D-GaIN/LPS-induced hepatocyte apoptosis by activating autophagy in vitro</p>

Cited by 75 publications

References 46 publications

Exosomes from normal cartilage endplate stem cells ameliorate intervertebral disc degeneration more effectively than exosomes from degenerated cartilage endplate stem cell by activating the AKT/autophagy pathway

Exosomes from normal cartilage endplate stem cells ameliorate intervertebral disc degeneration more effectively than exosomes from degenerated cartilage endplate stem cell by activating the AKT/autophagy pathway

Extracellular Vesicles in the Development of the Non-Alcoholic Fatty Liver Disease: An Update

Exosomal cargos modulate autophagy in recipient cells via different signaling pathways

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