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FGF21 Mediates Mesenchymal Stem Cell Senescence via Regulation of Mitochondrial Dynamics
Joint Authors
Liang, Xiaoting
Hong, Yimei
He, Haiwei
Jiang, Guojun
Zhang, Yuelin
Li, Xin
You, Wei
Han, Shuo
Lian, Qizhou
Fu, Qing-Ling
Source
Oxidative Medicine and Cellular Longevity
Issue
Vol. 2019, Issue 2019 (31 Dec. 2019), pp.1-13, 13 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2019-04-17
Country of Publication
Egypt
No. of Pages
13
Main Subjects
Abstract EN
Mesenchymal stem cell- (MSC-) based therapy is a novel strategy in regenerative medicine.
The functional and regenerative capacities of MSCs decline with senescence.
Nonetheless, the potential mechanisms that underlie their senescence are not fully understood.
This study was aimed at exploring the potential mechanisms of fibroblast growth factor 21 (FGF21) in the regulation of MSC senescence.
The senescence of MSCs was determined by senescence-associated β-galactosidase (SA-β-gal) staining.
The morphology and the level of mitochondrial reactive oxygen species (ROS) of MSCs were assessed by MitoTracker and Mito-Sox staining, respectively.
The expression of FGF21 and mitochondrial dynamics-related proteins was detected by Western blotting.
As MSCs were expanded in vitro, the expression of FGF21 decreased.
Depletion of FGF21 enhanced production of mitochondrial reactive oxidative species (ROS) and increased the senescence of early-passage MSCs whereas inhibition of ROS abolished these effects.
The senescent MSCs exhibited increased mitochondrial fusion and decreased mitochondrial fission.
Treatment of early-passage MSCs with FGF21 siRNA enhanced mitochondrial fusion and reduced mitochondrial fission.
Moreover, treatment of mitofusin2- (Mfn2-) siRNA inhibited depletion of FGF21-induced MSC senescence.
Furthermore, we demonstrated that depletion of FGF21-induced mitochondrial fusion was regulated by the AMPK signaling pathway.
Treatment with an AMPK activator, AICAR, abrogated the depletion of FGF21-induced senescence of MSCs by inhibiting mitochondrial fusion.
Compared with MSCs isolated from young donors, those derived from aged donors showed a lower level of FGF21 and a higher level of senescent activity.
Furthermore, overexpression of FGF21 in aged MSCs inhibited senescence.
Our study shows that FGF21, via the AMPK signaling pathway, regulates the senescence of MSCs by mediating mitochondrial dynamics.
Targeting FGF21 might represent a novel strategy to improve the quality and quantity of MSCs.
American Psychological Association (APA)
Li, Xin& Hong, Yimei& He, Haiwei& Jiang, Guojun& You, Wei& Liang, Xiaoting…[et al.]. 2019. FGF21 Mediates Mesenchymal Stem Cell Senescence via Regulation of Mitochondrial Dynamics. Oxidative Medicine and Cellular Longevity،Vol. 2019, no. 2019, pp.1-13.
https://search.emarefa.net/detail/BIM-1203874
Modern Language Association (MLA)
Li, Xin…[et al.]. FGF21 Mediates Mesenchymal Stem Cell Senescence via Regulation of Mitochondrial Dynamics. Oxidative Medicine and Cellular Longevity No. 2019 (2019), pp.1-13.
https://search.emarefa.net/detail/BIM-1203874
American Medical Association (AMA)
Li, Xin& Hong, Yimei& He, Haiwei& Jiang, Guojun& You, Wei& Liang, Xiaoting…[et al.]. FGF21 Mediates Mesenchymal Stem Cell Senescence via Regulation of Mitochondrial Dynamics. Oxidative Medicine and Cellular Longevity. 2019. Vol. 2019, no. 2019, pp.1-13.
https://search.emarefa.net/detail/BIM-1203874
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1203874