Mesenchymal stem cell conditioned medium attenuates oxidative stress injury in hepatocytes partly by regulating the miR-486-5p/PIM1 axis and the TGF-β/Smad pathway
This study investigated the role of microRNA (miRNA) miR-486-5p in oxidative stress injury in hepatocytes under the treatment of mesenchymal stem cell conditioned medium (MSC-CM). The oxidative stress injury in hepatocytes (L02) was induced by H2O2. Human umbilical cord blood MSC-CM (UCB-MSC-CM) was...
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Taylor & Francis Group
2021-01-01
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Series: | Bioengineered |
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Online Access: | http://dx.doi.org/10.1080/21655979.2021.1972196 |
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author | Ning Ma Shuo Li Chao Lin Xianbin Cheng Zihui Meng |
author_facet | Ning Ma Shuo Li Chao Lin Xianbin Cheng Zihui Meng |
author_sort | Ning Ma |
collection | DOAJ |
description | This study investigated the role of microRNA (miRNA) miR-486-5p in oxidative stress injury in hepatocytes under the treatment of mesenchymal stem cell conditioned medium (MSC-CM). The oxidative stress injury in hepatocytes (L02) was induced by H2O2. Human umbilical cord blood MSC-CM (UCB-MSC-CM) was prepared. The effects of UCB-MSC-CM on the proliferation, apoptosis, and inflammatory response in L02 cells were detected by Cell Counting Kit-8 (CCK-8) assay, flow cytometry analysis, and enzyme-linked immunosorbent assay (ELISA). Subsequently, the target of miR-486-5p was predicted using bioinformatics analysis, and the possible signaling pathway addressed by miR-486-5p was explored using western blot. We found that miR-486-5p expression was elevated following oxidative stress injury and was reduced after UCB-MSC-CM treatment. UCB-MSC-CM protected L02 cells against H2O2-induced injury by downregulation of miR-486-5p. Proviral integration site for Moloney murine leukemia virus 1 (PIM1) was verified to be targeted by miR-486-5p. UCB-MSC-CM upregulated the expression of PIM1 reduced by H2O2 in L02 cells. Additionally, silencing PIM1 attenuated the protective effects of miR-486-5p downregulation against oxidative stress injury. We further demonstrated that UCB-MSC-CM inhibited the TGF-β/Smad signaling in H2O2-treated L02 cells by the miR-486-5p/PIM1 axis. Overall, UCB-MSC-CM attenuates oxidative stress injury in hepatocytes by downregulating miR-486-5p and upregulating PIM1, which may be related to the inhibition of TGF-β/Smad pathway. |
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issn | 2165-5979 2165-5987 |
language | English |
last_indexed | 2024-04-11T20:38:04Z |
publishDate | 2021-01-01 |
publisher | Taylor & Francis Group |
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series | Bioengineered |
spelling | doaj.art-a1eb31982abb45918eff09304b01f6bd2022-12-22T04:04:18ZengTaylor & Francis GroupBioengineered2165-59792165-59872021-01-011216434644710.1080/21655979.2021.19721961972196Mesenchymal stem cell conditioned medium attenuates oxidative stress injury in hepatocytes partly by regulating the miR-486-5p/PIM1 axis and the TGF-β/Smad pathwayNing Ma0Shuo Li1Chao Lin2Xianbin Cheng3Zihui Meng4China-Japan Union Hospital of Jilin UniversityChina-Japan Union Hospital of Jilin UniversityChina-Japan Union Hospital of Jilin UniversityChina-Japan Union Hospital of Jilin UniversityChina-Japan Union Hospital of Jilin UniversityThis study investigated the role of microRNA (miRNA) miR-486-5p in oxidative stress injury in hepatocytes under the treatment of mesenchymal stem cell conditioned medium (MSC-CM). The oxidative stress injury in hepatocytes (L02) was induced by H2O2. Human umbilical cord blood MSC-CM (UCB-MSC-CM) was prepared. The effects of UCB-MSC-CM on the proliferation, apoptosis, and inflammatory response in L02 cells were detected by Cell Counting Kit-8 (CCK-8) assay, flow cytometry analysis, and enzyme-linked immunosorbent assay (ELISA). Subsequently, the target of miR-486-5p was predicted using bioinformatics analysis, and the possible signaling pathway addressed by miR-486-5p was explored using western blot. We found that miR-486-5p expression was elevated following oxidative stress injury and was reduced after UCB-MSC-CM treatment. UCB-MSC-CM protected L02 cells against H2O2-induced injury by downregulation of miR-486-5p. Proviral integration site for Moloney murine leukemia virus 1 (PIM1) was verified to be targeted by miR-486-5p. UCB-MSC-CM upregulated the expression of PIM1 reduced by H2O2 in L02 cells. Additionally, silencing PIM1 attenuated the protective effects of miR-486-5p downregulation against oxidative stress injury. We further demonstrated that UCB-MSC-CM inhibited the TGF-β/Smad signaling in H2O2-treated L02 cells by the miR-486-5p/PIM1 axis. Overall, UCB-MSC-CM attenuates oxidative stress injury in hepatocytes by downregulating miR-486-5p and upregulating PIM1, which may be related to the inhibition of TGF-β/Smad pathway.http://dx.doi.org/10.1080/21655979.2021.1972196oxidative injuryucb-msc-cmmir-486-5ppim1tgf-β/smad pathway |
spellingShingle | Ning Ma Shuo Li Chao Lin Xianbin Cheng Zihui Meng Mesenchymal stem cell conditioned medium attenuates oxidative stress injury in hepatocytes partly by regulating the miR-486-5p/PIM1 axis and the TGF-β/Smad pathway Bioengineered oxidative injury ucb-msc-cm mir-486-5p pim1 tgf-β/smad pathway |
title | Mesenchymal stem cell conditioned medium attenuates oxidative stress injury in hepatocytes partly by regulating the miR-486-5p/PIM1 axis and the TGF-β/Smad pathway |
title_full | Mesenchymal stem cell conditioned medium attenuates oxidative stress injury in hepatocytes partly by regulating the miR-486-5p/PIM1 axis and the TGF-β/Smad pathway |
title_fullStr | Mesenchymal stem cell conditioned medium attenuates oxidative stress injury in hepatocytes partly by regulating the miR-486-5p/PIM1 axis and the TGF-β/Smad pathway |
title_full_unstemmed | Mesenchymal stem cell conditioned medium attenuates oxidative stress injury in hepatocytes partly by regulating the miR-486-5p/PIM1 axis and the TGF-β/Smad pathway |
title_short | Mesenchymal stem cell conditioned medium attenuates oxidative stress injury in hepatocytes partly by regulating the miR-486-5p/PIM1 axis and the TGF-β/Smad pathway |
title_sort | mesenchymal stem cell conditioned medium attenuates oxidative stress injury in hepatocytes partly by regulating the mir 486 5p pim1 axis and the tgf β smad pathway |
topic | oxidative injury ucb-msc-cm mir-486-5p pim1 tgf-β/smad pathway |
url | http://dx.doi.org/10.1080/21655979.2021.1972196 |
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