Stem Cell-Derived Exosomes Prevent Aging-Induced Cardiac Dysfunction through a Novel Exosome/lncRNA MALAT1/NF-κB/TNF-α Signaling Pathway. (8th April 2019)

• Record Type: Journal Article
• Authors: Zhu, Bao; Zhang, Lulu; Liang, Chun; Liu, Bin; Pan, Xiangbin; Wang, Yanli; Zhang, Yuqing; Zhang, Yu; Xie, Wenping; Yan, Bing; Liu, Feng; Yip, Hon-Kan; Yu, Xi-yong; Li, Yangxin
• Other Names: Bihl Ji C. Academic Editor.
• Is Part Of: Oxidative medicine and cellular longevity. Volume 2019(2019)
• Publication Date: 2019-04-08
• Subjects: Oxidative stress -- Periodicals; Cells -- Aging -- Periodicals; Cells -- Aging; Oxidative stress; Oxidative Stress -- Periodicals; Cell Aging -- Periodicals; Periodicals; 611.0181
• DOI: 10.1155/2019/9739258
• Languages: English
• ISSNs: 1942-0900

Abstract

Abstract : Aging is a risk factor for cardiovascular disease, and there is no effective therapeutic approach to alleviate this condition. NF- κ B and TNF- α have been implicated in the activation of the aging process, but the signaling molecules responsible for the inactivation of NF- κ B and TNF- α remain unknown. Exosomes have been reported to improve heart functions by releasing miRNA. Recent studies suggest that lncRNAs are more tissue-specific and developmental stage-specific compared to miRNA. However, the role of lncRNA in exosome-mediated cardiac repair has not been explored. In the present study, we focused on metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), which is an lncRNA associated with cell senescence. We discovered that human umbilical cord mesenchymal stem cell- (UMSC-) derived exosomes prevent aging-induced cardiac dysfunction. Silencer RNA against lncRNA MALAT1 blocked the beneficial effects of exosomes. In summary, we discovered that UMSC-derived exosomes prevent aging-induced cardiac dysfunction by releasing novel lncRNA MALAT1, which in turn inhibits the NF- κ B/TNF- α signaling pathway. These findings will lead to the development of therapies that delay aging and progression of age-related diseases.