NDLI: Enpp1 deficiency caused chondrocyte apoptosis by inhibiting AMPK signaling pathway

Content Provider	Springer Nature : BioMed Central
Author	Gao, Zhiqiang Wang, Qiang Guo, Kai Li, Xinhua Huang, Yufeng
Abstract	Objective and background The deficiency of ectonucleotide pyrophosphatase/phosphodiesterase 1 (Enpp1) causes the phenotype similar to knee osteoarthritis (OA). However, the molecular mechanism is poorly understood. Method The global deletion of Enpp1 (Enpp1−/−) mice was created to analyze the role of Enpp1 in the progress of knee OA. The apoptosis, proliferation and chondrogenic differentiation ability of chondrocytes from wild-type (WT) and Enpp1−/− joints were compared. According to the results of high-throughput quantitative molecular measurements, the proteins of chondrocytes from WT and Enpp1−/− mice were used to explore the mechanism of Enpp1 deficiency-associated knee OA. Result In Enpp1−/− knee joints, we found significant chondrocyte apoptosis and proteomic results showed that abnormal expression of AMP-activated protein kinase (AMPK) signaling pathway may contribute to this phenotype. In primary chondrocyte cultures in vitro, Enpp1 deletion dramatically enhancing chondrocyte apoptosis. Meanwhile, we found Enpp1 deletion inhibits the phosphorylation of AMPK (P-AMPK). We also found that decreased level of P-AMPK and chondrocyte apoptosis, which are caused by Enpp1 deficiency, can be reversed by Acadesine (AICAR), the activator of AMPK. Conclusion Consequently, Enpp1 deficiency plays an essential role in knee OA by regulating AMPK signaling pathway.
Related Links	https://josr-online.biomedcentral.com/counter/pdf/10.1186/s13018-023-03923-1.pdf
Ending Page	10
Page Count	10
Starting Page	1
File Format	HTM / HTML
DOI	10.1186/s13018-023-03923-1
Journal	Journal of Orthopaedic Surgery and Research
Issue Number	1
Volume Number	18
Language	English
Publisher	BioMed Central
Publisher Date	2023-06-27
Access Restriction	Open
Subject Keyword	Orthopedics Surgical Orthopedics Enpp1 Osteoarthritis Apoptosis AMPK AICAR
Content Type	Text
Resource Type	Article
Subject	Surgery Orthopedics and Sports Medicine
Journal Impact Factor	2.8/2023
5-Year Journal Impact Factor	3/2023

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