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Myeloid-derived growth factor inhibits inflammation and alleviates endothelial injury and atherosclerosis in mice
Whether bone marrow modulates systemic metabolism remains unknown. Here, we found that (i) myeloid cell–specific myeloid-derived growth factor (MYDGF) deficiency exacerbated vascular inflammation, adhesion responses, endothelial injury, and atherosclerosis in vivo. (ii) Myeloid cell–specific MYDGF r...
Autores principales: | , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
American Association for the Advancement of Science
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8139583/ https://www.ncbi.nlm.nih.gov/pubmed/34020949 http://dx.doi.org/10.1126/sciadv.abe6903 |
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author | Meng, Biying Li, Yixiang Ding, Yan Xu, Xiaoli Wang, Li Guo, Bei Zhu, Biao Zhang, Jiajia Xiang, Lin Dong, Jing Liu, Min Xiang, Lingwei Xiang, Guangda |
author_facet | Meng, Biying Li, Yixiang Ding, Yan Xu, Xiaoli Wang, Li Guo, Bei Zhu, Biao Zhang, Jiajia Xiang, Lin Dong, Jing Liu, Min Xiang, Lingwei Xiang, Guangda |
author_sort | Meng, Biying |
collection | PubMed |
description | Whether bone marrow modulates systemic metabolism remains unknown. Here, we found that (i) myeloid cell–specific myeloid-derived growth factor (MYDGF) deficiency exacerbated vascular inflammation, adhesion responses, endothelial injury, and atherosclerosis in vivo. (ii) Myeloid cell–specific MYDGF restoration attenuated vascular inflammation, adhesion responses and leukocyte homing and alleviated endothelial injury and atherosclerosis in vivo. (iii) MYDGF attenuated endothelial inflammation, apoptosis, permeability, and adhesion responses induced by palmitic acid in vitro. (iv) MYDGF alleviated endothelial injury and atherosclerosis through mitogen-activated protein kinase kinase kinase kinase 4 (MAP4K4)/nuclear factor κB (NF-κB) signaling. Therefore, we concluded that MYDGF inhibits endothelial inflammation and adhesion responses, blunts leukocyte homing, protects against endothelial injury and atherosclerosis in a manner involving MAP4K4/NF-κB signaling, and serves as a cross-talk factor between bone marrow and arteries to regulate the pathophysiology of arteries. Bone marrow functions as an endocrine organ and serves as a potential therapeutic target for metabolic disorders. |
format | Online Article Text |
id | pubmed-8139583 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | American Association for the Advancement of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-81395832021-05-26 Myeloid-derived growth factor inhibits inflammation and alleviates endothelial injury and atherosclerosis in mice Meng, Biying Li, Yixiang Ding, Yan Xu, Xiaoli Wang, Li Guo, Bei Zhu, Biao Zhang, Jiajia Xiang, Lin Dong, Jing Liu, Min Xiang, Lingwei Xiang, Guangda Sci Adv Research Articles Whether bone marrow modulates systemic metabolism remains unknown. Here, we found that (i) myeloid cell–specific myeloid-derived growth factor (MYDGF) deficiency exacerbated vascular inflammation, adhesion responses, endothelial injury, and atherosclerosis in vivo. (ii) Myeloid cell–specific MYDGF restoration attenuated vascular inflammation, adhesion responses and leukocyte homing and alleviated endothelial injury and atherosclerosis in vivo. (iii) MYDGF attenuated endothelial inflammation, apoptosis, permeability, and adhesion responses induced by palmitic acid in vitro. (iv) MYDGF alleviated endothelial injury and atherosclerosis through mitogen-activated protein kinase kinase kinase kinase 4 (MAP4K4)/nuclear factor κB (NF-κB) signaling. Therefore, we concluded that MYDGF inhibits endothelial inflammation and adhesion responses, blunts leukocyte homing, protects against endothelial injury and atherosclerosis in a manner involving MAP4K4/NF-κB signaling, and serves as a cross-talk factor between bone marrow and arteries to regulate the pathophysiology of arteries. Bone marrow functions as an endocrine organ and serves as a potential therapeutic target for metabolic disorders. American Association for the Advancement of Science 2021-05-21 /pmc/articles/PMC8139583/ /pubmed/34020949 http://dx.doi.org/10.1126/sciadv.abe6903 Text en Copyright © 2021 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works. Distributed under a Creative Commons Attribution NonCommercial License 4.0 (CC BY-NC). https://creativecommons.org/licenses/by-nc/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial license (https://creativecommons.org/licenses/by-nc/4.0/) , which permits use, distribution, and reproduction in any medium, so long as the resultant use is not for commercial advantage and provided the original work is properly cited. |
spellingShingle | Research Articles Meng, Biying Li, Yixiang Ding, Yan Xu, Xiaoli Wang, Li Guo, Bei Zhu, Biao Zhang, Jiajia Xiang, Lin Dong, Jing Liu, Min Xiang, Lingwei Xiang, Guangda Myeloid-derived growth factor inhibits inflammation and alleviates endothelial injury and atherosclerosis in mice |
title | Myeloid-derived growth factor inhibits inflammation and alleviates endothelial injury and atherosclerosis in mice |
title_full | Myeloid-derived growth factor inhibits inflammation and alleviates endothelial injury and atherosclerosis in mice |
title_fullStr | Myeloid-derived growth factor inhibits inflammation and alleviates endothelial injury and atherosclerosis in mice |
title_full_unstemmed | Myeloid-derived growth factor inhibits inflammation and alleviates endothelial injury and atherosclerosis in mice |
title_short | Myeloid-derived growth factor inhibits inflammation and alleviates endothelial injury and atherosclerosis in mice |
title_sort | myeloid-derived growth factor inhibits inflammation and alleviates endothelial injury and atherosclerosis in mice |
topic | Research Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8139583/ https://www.ncbi.nlm.nih.gov/pubmed/34020949 http://dx.doi.org/10.1126/sciadv.abe6903 |
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