Exosomes derived miR-126 attenuates oxidative stress and apoptosis from ischemia and reperfusion injury by targeting ERRFI1

Wang, Wenyi; Zheng, Yashu; Wang, Miao; Yan, Meiling; Jiang, Jian; Li, Zhigang

doi:10.1016/j.gene.2018.12.044

Cited by 44 publications

(39 citation statements)

References 30 publications

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“…Defensive antioxidants, such as SOD and GSH-Px, can ameliorate the elevation of oxidants and therefore protect brain tissues against ROS cytotoxicity (35). miR-126 has been demonstrated to reduce oxidative stress and apoptosis in I/R injury (36). Similarly, the present study revealed that miR-126 mimics reversed the OGD/R-induced increase in ROS generation and MDA content (a major marker of lipid peroxidation caused by oxidative stress), and the OGD/R-induced decrease in SOD and GSH-Px activities in HUVECs.…”

Section: Discussionmentioning

confidence: 99%

miR‑126 overexpression attenuates oxygen‑glucose deprivation/reperfusion injury by inhibiting oxidative stress and inflammatory response via the activation of SIRT1/Nrf2 signaling pathway in human umbilical vein endothelial cells

Yang

Wang

2020

Mol Med Rep

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Section: Discussionmentioning

confidence: 99%

miR‑126 overexpression attenuates oxygen‑glucose deprivation/reperfusion injury by inhibiting oxidative stress and inflammatory response via the activation of SIRT1/Nrf2 signaling pathway in human umbilical vein endothelial cells

Yang

Wang

2020

Mol Med Rep

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“…As reported, Mig-6 could be regulated by certain miRNAs [20][21][22][23], Especially miR-589-5p and miR-374a, regulated the proliferation of HCC cells by targeting Mig-6 [24,25]. These studies stimulated the interest in exploring whether Mig-6 could affect the changes in miRNAs.…”

Section: Discussionmentioning

confidence: 88%

WITHDRAWN: Mig-6 Promotes the Apoptosis and Inhibits of the Flux of Autophagy in HCC Cell Lines Through Modulating Mig-6/miR-193a-3p/TGF-β2 Axis

Tian

Hong

et al. 2020

Preprint

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Abstract Background:Mitogen-inducible gene 6 (Mig-6) is a tumor suppressor gene that plays an important role in many types of cancers by interacting with EGFR. Thus far, little is known about the molecular mechanism of Mig-6 in hepatocellular carcinoma (HCC). Also, the relationship between Mig-6 and miRNAs needs to be elucidated. Therefore, this study first aimed to find whether Mig-6 could promote apoptosis and inhibition of the flux of autophagy by its downstream miRNA in HCC cell lines. Methods: Two cell lines, HepG2and HLE, were used in this study. Mig-6 overexpression and knockdown models , miR-193a mimics and inhibitors models,were established. MiRNA microarray profiling were used to verified Mig-6 regulated- miRNA. Real-time PCR, Western blot analysis were carried out to detect RNA and protein expression.Evaluation of fluorescent LC3 puncta and cell fow cytometer assay were used to test the autophagy and apoptosis respectively. Results: Mig-6 induced the apoptosis and reduced the autophagy of HCC cell lines. MiR-193a-3p is a Mig-6-regulated miRNA in Mig-6 overexpression model, and miR-193a-3p affected the apoptosis and autophagy of HCC cells by regulating the expression of TGF-β2. Additionally, the relationship between Mig-6 and transforming growth factor TGF-β2 was explored in depth for the first time.Conclusion:These findings revealed an important regulatory axis Mig-6/miR-193a-3p/TGF-β2 in the apoptosis and autophagy of HCC cells, providing a novel insight into the therapeutic target in HCC.

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“…Interestingly, endothelial specific microRNA (miR-126) play an important role in ischemic reperfusion injury by promoting neovascularization (arteriogenesis) in response to vessel injury and/or tissue hypoxia for improving cell survival [ 55 , 56 ]. Recent insights underline the precise role of miR-126 in reducing apoptosis and fibrosis by promoting angiogenesis of endothelial cells via the PI3K/eNOS/NO pathway, suppressing oxidative stress and stabilizing mitochondrial membrane potential in vivo [ 57 ]. Furthermore, miR-126 could act as a diagnostic and screening biomarker for liver neoplastic disease as it has been overexpressed in the serum of dogs with hepatocellular carcinoma [ 58 ] due to its critical roles on tumor angiogenesis [ 59 ].…”

Section: Discussionmentioning

confidence: 99%

Clinical Characteristics, Serum Biochemical Changes, and Expression Profile of Serum Cfa-miRNAs in Dogs Confirmed to Have Congenital Portosystemic Shunts Accompanied by Liver Pathologies

El-Sebaey

Abramov

Abdelhamid

2020

Veterinary Sciences

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Computed tomography angiography (CTA) and biochemical parameters cannot specify liver pathologies in dogs with congenital portosystemic shunts (CPSS) that are easily determined by invasive histopathology. This study aims to assess the possibility of using circulating serum canine familiaris (cfa) microRNAs (miRNAs) as novel non-invasive serum-based fingerprints for liver injuries associated with various morphologies of extrahepatic and intrahepatic portosystemic shunts (EHPSS and IHPSS). Data were obtained from 12 healthy dogs and 84 dogs confirmed to have EHPSS (splenocaval, splenophrenic, splenoazygos, right gastrocaval (RGC), right gastrocaval with caudal loop (RGC–CL)) and IHPSS (right divisional and left divisional) using CTA. Hepatic pathologies were determined by histopathology. Serum expression of miRNAs was assessed by real-time polymerase chain reaction. Based on the nature of liver injuries in each shunt type, cfa-miR-122 was significantly upregulated in all CPSS groups. Meanwhile, serums cfa-miR-34a and 21 were not significantly expressed in splenophrenic or splenoazygos groups, but they were extensively upregulated in splenocaval, RGC, RGC–CL groups and less frequently in right or left divisional groups. Also, serum cfa-miR126 was significantly upregulated in both IHPSS groups but less significantly expressed in RGC, RGC–CL, and splenocaval groups. Overall, estimated cfa-miRNAs could serve as novel biomarkers to mirror the histopathological and molecular events within the liver in each shunt type.

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Exosomes derived miR-126 attenuates oxidative stress and apoptosis from ischemia and reperfusion injury by targeting ERRFI1

Cited by 44 publications

References 30 publications

miR‑126 overexpression attenuates oxygen‑glucose deprivation/reperfusion injury by inhibiting oxidative stress and inflammatory response via the activation of SIRT1/Nrf2 signaling pathway in human umbilical vein endothelial cells

miR‑126 overexpression attenuates oxygen‑glucose deprivation/reperfusion injury by inhibiting oxidative stress and inflammatory response via the activation of SIRT1/Nrf2 signaling pathway in human umbilical vein endothelial cells

WITHDRAWN: Mig-6 Promotes the Apoptosis and Inhibits of the Flux of Autophagy in HCC Cell Lines Through Modulating Mig-6/miR-193a-3p/TGF-β2 Axis

Clinical Characteristics, Serum Biochemical Changes, and Expression Profile of Serum Cfa-miRNAs in Dogs Confirmed to Have Congenital Portosystemic Shunts Accompanied by Liver Pathologies

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