![](/images/graphics-bg.png)
Rapamycin-Induced Autophagy Promotes the Chondrogenic Differentiation of Synovium-Derived Mesenchymal Stem Cells in the Temporomandibular Joint in Response to IL-1β
Joint Authors
Liu, Wenjing
Luo, Haiyun
Wang, Ruolan
Kang, Yiyuan
Liao, Wenting
Sun, Yangpeng
Chen, Guodong
Shao, Longquan
Source
Issue
Vol. 2020, Issue 2020 (31 Dec. 2020), pp.1-12, 12 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2020-10-22
Country of Publication
Egypt
No. of Pages
12
Main Subjects
Abstract EN
Cartilage defects in temporomandibular disorders (TMD) lead to chronic pain and seldom heal.
Synovium-derived mesenchymal stem cells (SMSCs) exhibit superior chondrogenesis and have become promising seed cells for cartilage tissue engineering.
However, local inflammatory conditions that affect the repair of articular cartilage by SMSCs present a challenge, and the specific mechanism through which the function remains unclear.
Thus, it is important to explore the chondrogenesis of SMSCs under inflammatory conditions of TMD such that they can be used more effectively in clinical treatment.
In this study, we obtained SMSCs from TMD patients with severe cartilage injuries.
In response to stimulation with IL-1β, which is well known as one of the most prevalent cytokines in TMD, MMP13 expression increased, while that of SOX9, aggrecan, and collagen II decreased during chondrogenic differentiation.
At the same time, IL-1β upregulated the expression of mTOR and decreased the ratio of LC3-II/LC3-I and the formation of autophagosomes.
Further study revealed that rapamycin pretreatment promoted the migration of SMSCs and the expression of chondrogenesis-related markers in the presence of IL-1β by inducing autophagy.
3-Benzyl-5-((2-nitrophenoxy)methyl)-dihydrofuran-2(3H)-one (3BDO), a new activator of mTOR, inhibited autophagy and increased the expression of p-GSK3βser9 and β-catenin, simulating the effect of IL-1β stimulation.
Furthermore, rapamycin reduced the expression of mTOR, whereas the promotion of LC3-II/LC3-I was blocked by the GSK3β inhibitor TWS119.
Taken together, these results indicate that rapamycin enhances the chondrogenesis of SMSCs by inducing autophagy, and GSK3β may be an important regulator in the process of rapamycin-induced autophagy.
Thus, inducing autophagy may be a useful approach in the chondrogenic differentiation of SMSCs in the inflammatory microenvironment and may represent a novel TMD treatment.
American Psychological Association (APA)
Liu, Wenjing& Luo, Haiyun& Wang, Ruolan& Kang, Yiyuan& Liao, Wenting& Sun, Yangpeng…[et al.]. 2020. Rapamycin-Induced Autophagy Promotes the Chondrogenic Differentiation of Synovium-Derived Mesenchymal Stem Cells in the Temporomandibular Joint in Response to IL-1β. BioMed Research International،Vol. 2020, no. 2020, pp.1-12.
https://search.emarefa.net/detail/BIM-1133648
Modern Language Association (MLA)
Liu, Wenjing…[et al.]. Rapamycin-Induced Autophagy Promotes the Chondrogenic Differentiation of Synovium-Derived Mesenchymal Stem Cells in the Temporomandibular Joint in Response to IL-1β. BioMed Research International No. 2020 (2020), pp.1-12.
https://search.emarefa.net/detail/BIM-1133648
American Medical Association (AMA)
Liu, Wenjing& Luo, Haiyun& Wang, Ruolan& Kang, Yiyuan& Liao, Wenting& Sun, Yangpeng…[et al.]. Rapamycin-Induced Autophagy Promotes the Chondrogenic Differentiation of Synovium-Derived Mesenchymal Stem Cells in the Temporomandibular Joint in Response to IL-1β. BioMed Research International. 2020. Vol. 2020, no. 2020, pp.1-12.
https://search.emarefa.net/detail/BIM-1133648
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1133648