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Melatonin activates ABCA1 via the BiP/NRF1 pathway to suppress high-cholesterol-induced apoptosis of mesenchymal stem cells
DC Field | Value | Language |
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dc.contributor.author | Kim, Jun Sung | - |
dc.contributor.author | Jung, Young Hyun | - |
dc.contributor.author | Lee, Hyun Jik | - |
dc.contributor.author | Chae, Chang Woo | - |
dc.contributor.author | Choi, Gee Euhn | - |
dc.contributor.author | Lim, Jae Ryong | - |
dc.contributor.author | Kim, Seo Yihl | - |
dc.contributor.author | Lee, Joo Eun | - |
dc.contributor.author | Han, Ho Jae | - |
dc.date.accessioned | 2021-05-11T00:24:14Z | - |
dc.date.available | 2021-05-11T09:30:44Z | - |
dc.date.issued | 2021-02-05 | - |
dc.identifier.citation | Stem Cell Research & Therapy. 2021 Feb 05;12(1):114 | - |
dc.identifier.uri | https://doi.org/10.1186/s13287-021-02181-4 | - |
dc.identifier.uri | https://hdl.handle.net/10371/174232 | - |
dc.description.abstract | Abstract
Background Retarded wound healing in patients with obesity contributes to a risk of complications associated with vascular insufficiency and oxidative stress. The high cholesterol levels of patients with obesity are associated with apoptosis of engrafted umbilical cord blood-derived mesenchymal stem cells (UCB-MSCs). Melatonin contributes to the prevention of cholesterol accumulation in patients with obesity via a mechanism that is poorly understood. We therefore investigated the regulatory mechanism of melatonin in cholesterol-induced apoptosis. Methods The protective effects of melatonin on cholesterol-induced apoptosis were investigated in UCB-MSCs. We used a mouse model of induced obesity to show that melatonin treatment restored the survival rate of transplanted UCB-MSCs and their wound-healing capacity. The mean values of the treatment groups were compared with those of the control group using Students t test, and differences among three or more groups were analyzed using one-way analysis of variance with Dunnetts multiple comparison test. Results Melatonin treatment increased the expression of ATP-binding cassette subfamily A member 1 (ABCA1), which reduced cholesterol accumulation and cholesterol-induced apoptosis. The mouse skin wound healing model showed that melatonin treatment restored the survival rate of transplanted UCB-MSCs and the wound-healing capacity of obese mice. Melatonin inhibited the expression of binding immunoglobulin protein (BiP) through the regulation of MT2/Sp1-dependent microRNA-597-5p. Melatonin decreased the co-localization of BiP with nuclear factor erythroid 2-related factor 1 (NRF1), which resulted in increased ABCA1 expression. Conclusion Melatonin induced the efflux of intracellular cholesterol through ABCA1 to decrease apoptosis of UCB-MSCs via an MT2-dependent BiP/NRF1 pathway. | - |
dc.title | Melatonin activates ABCA1 via the BiP/NRF1 pathway to suppress high-cholesterol-induced apoptosis of mesenchymal stem cells | - |
dc.type | Article | - |
dc.contributor.AlternativeAuthor | 정영현 | - |
dc.contributor.AlternativeAuthor | 이현직 | - |
dc.contributor.AlternativeAuthor | 채창우 | - |
dc.contributor.AlternativeAuthor | 최지은 | - |
dc.contributor.AlternativeAuthor | 임재룡 | - |
dc.contributor.AlternativeAuthor | 김서일 | - |
dc.contributor.AlternativeAuthor | 이주은 | - |
dc.contributor.AlternativeAuthor | 한호재 | - |
dc.author.alternative | 김준성 | - |
dc.language.rfc3066 | en | - |
dc.rights.holder | The Author(s) | - |
dc.date.updated | 2021-02-15T10:31:35Z | - |
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