miR-30b inhibits autophagy to alleviate hepatic ischemia-reperfusion injury<i>via</i>decreasing the Atg12-Atg5 conjugate

Li, Shipeng

doi:10.3748/wjg.v22.i18.4501

Cited by 35 publications

(22 citation statements)

References 28 publications

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“…The beneficial effect of BM-MSCs was further confirmed by Fu et al (25), who documented that the hepatoprotection provided by BM-MSCs following I/R injury was dependent on the inhibition of hepatocellular apoptosis and the stimulation of N-acetyltransferase 8 regeneration in vivo or in vitro. Consistent with these observations, the present study confirmed that BM-MSCs had beneficial effects against liver I/R injury in vivo by observing levels of ALT/AST and alterations in histomorphology that were consistent with certain published papers (41,42). Previous studies revealed that MSCs attenuated I/R injury in solid organs through various complex mechanisms, including an anti-inflammatory reaction (12,40), angiogenesis (43), anti-oxidative stress (44,45), and immunomodulation (46).…”

Section: Discussionsupporting

confidence: 91%

BM‑MSCs protect against liver ischemia/reperfusion injury via HO‑1 mediated autophagy

Wang

Zhou

et al. 2018

Mol Med Report

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Ischemia/reperfusion (I/R) injury is considered to be a contributing factor in liver injury following major hepatic resection or liver transplantation. Bone marrow mesenchymal stem cells (BM‑MSCs) have the potential to protect against liver I/R injury; however, the precise mechanisms have not been completely elucidated. Autophagy serves an important role in protecting against various injuries, including I/R injury. The present study aimed to determine the role of autophagy and its potential regulatory mechanism in BM‑MSC‑mediated protection against liver I/R injury in rats. The results demonstrated that BM‑MSCs mitigated I/R injury and enhanced autophagy in vivo. In addition, inhibition of autophagy by 3‑methyladenine reversed the positive effects of BM‑MSCs. Furthermore, heme oxygenase‑1 (HO‑1) expression was promoted by BM‑MSCs. Using zinc protoporphyrin IX to inhibit HO‑1 demonstrated that HO‑1 was important for the promotion of autophagy. In conclusion, the present study revealed that BM‑MSCs protected against liver I/R injury via the promotion of HO‑1‑mediated autophagy.

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Section: Discussionsupporting

confidence: 91%

BM‑MSCs protect against liver ischemia/reperfusion injury via HO‑1 mediated autophagy

Wang

Zhou

et al. 2018

Mol Med Report

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“…AML12 cells were cultured in six well plates to 60‐70% confluence. The cells were transfected with tandem GFP‐RFP‐LC3 adenovirus (Hanbio, Shanghai, China) according to the GFP‐RFP‐LC3 instruction manual to further confrm autophagy induction …”

Section: Methodsmentioning

confidence: 99%

Stat3‐Atg5 signal axis inducing autophagy to alleviate hepatic ischemia‐reperfusion injury

Han

Zhao

et al. 2017

J of Cellular Biochemistry

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In performing our experiment, impaired autophagy increased hepatocellular damage during the reperfusion period. It was demonstrated by the effect of blocking autophagy using bafilomycin A1 or knocking Atg5 gene out reduces the anti-apoptotic effect of Stat3. Here we focus on the role of signal transducer and activator of transcription 3 (Stat3) in regulating autophagy to alleviate hepatic IRI. We found that Stat3 was up-regulated during hepatic IRI and was associated with an activation of the autophagic signaling pathway. This increased Stat3 expression, which was allied with high autophagic activity, alleviated liver damage to IR, an effect which was abrogated by Stat3 epletion as demonstrated in both in vivo and in vitro methods. The levels of Atg5 protein were decreased when Stat3 was inhibited by HO 3867 or siStat3. We conclude that Stat3 appeared to exert a pivotal role in hepatic IRI, by activating autophagy to alleviate hepatic IRI, and Atg5 was required for this process. The identification of this novel pathway, that links expression levels of Stat3 with Atg5-mediated autophagy, may provide new insights for the generation of novel protective therapies directed against hepatic IRI.

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“…For example, miR-30b, for which a predicted target site resides in the 3ʹ-UTR of autophagy-associated gene 12 (Atg12), has been shown to modulate autophagy in hepatic ischemia-reperfusion injury [24]. The current study aimed to determine the potential role of miR-30b in TNF-α-induced apoptosis, autophagy and differentiation in the ATDC5 chondrogenic cell line.…”

Section: Discussionmentioning

confidence: 99%

“…Recent findings have indicated some novel roles for miRNAs in the regulation of autophagy [22,23]. The 3ʹ-UTR of autophagy-associated gene 12 (Atg12) was reported to contain a predicted target site for miRNA-30b (miR-30b) and this miRNA has been shown to modulate autophagy in hepatic ischemia-reperfusion injury [24].…”

Section: Introductionmentioning

confidence: 99%

AntimiR-30b Inhibits TNF-α Mediated Apoptosis and Attenuated Cartilage Degradation through Enhancing Autophagy

Chen

Jin

2016

Cell Physiol Biochem

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Objective: Cell death plays an important role in the pathology associated with inflammatory diseases such as osteoarthritis. It has been reported that autophagy can protect cells against tumour necrosis factor-α (TNF-α)-induced apoptosis. This study aimed to determine the potential role of microRNA-30b (miR-30b) in TNF-α-induced apoptosis, autophagy and differentiation in the chondrogenic ADTC5 cell line. Methods: To analyse the effect of TNF-α on the viability of ADTC5 cells, cell counting kit-8 and Hoechst 33342 staining were employed and the expression levels of caspase-3 and -9 were assessed. Autophagy was examined by analysing the levels of LC3B-II and p62 and quantitating GFP-LC3B by fluorescence microscopy. A luciferase reporter assay investigated the putative binding sites of miR-30b. The effects of miR-30b and antimiR-30b on autophagy, apoptosis and osteogenic differentiation of TNF-α-treated cells were determined by autophagosome, apoptosis and alkaline phosphatase assays, respectively. Results: TNF-α exposure decreased cell viability, increased apoptosis and positively regulated autophagy in ADTC5 cells. A direct interaction was detected between miR-30b and the mRNA 3ʹ-UTRs of autophagy genes BECN1 and ATG5. Overexpression of miR-30b downregulated autophagy genes and upregulated pro-apoptotic gene expression in TNF-α-treated cells, while treatment with antimiR-30b had the inverse effect. Overexpression of miR-30b also downregulated ECM degradation and anti-miR-30b reverse TNF-α-induced ECM degradation. Conclusions: Anti-miR-30b enhanced autophagy and attenuated cartilage degradation and played a protective role in TNF-α-induced apoptosis of ATDC5 cells. Anti-miR-30b may therefore elevate cellular survival during inflammation and has therapeutic potential for inflammatory diseases such as osteoarthritis.

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miR-30b inhibits autophagy to alleviate hepatic ischemia-reperfusion injuryviadecreasing the Atg12-Atg5 conjugate

Abstract: miR-30b inhibited autophagy to alleviate hepatic ischemia-reperfusion injury via decreasing the Atg12-Atg5 conjugate.

Cited by 35 publications

References 28 publications

BM‑MSCs protect against liver ischemia/reperfusion injury via HO‑1 mediated autophagy

BM‑MSCs protect against liver ischemia/reperfusion injury via HO‑1 mediated autophagy

Stat3‐Atg5 signal axis inducing autophagy to alleviate hepatic ischemia‐reperfusion injury

AntimiR-30b Inhibits TNF-α Mediated Apoptosis and Attenuated Cartilage Degradation through Enhancing Autophagy

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