Tissue & cell · 2026
ENTR1 ameliorates osteoarthritis through decreasing FAS expression by binding PTPN13.
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Gao Nan, Guo Qiushuang, Zhao Shuaiqi, Ren Huiping, Lan Jing
Аннотация
PURPOSE: This study aimed to explore the effects and mechanisms of endosome-associated trafficking regulator 1 (ENTR1) in osteoarthritis (OA), thereby providing a novel therapeutic target.
METHODS: We established OA rat model via the destabilization of the medial meniscus (DMM) surgery and OA cell model via IL-1β-stimulated ATDC5 cells. HE and safranin O/fast green staining were employed to assess the pathological changes of cartilage tissues in rats. Moreover, TUNEL staining was applied to examine chondrocyte apoptosis in rat cartilage tissues. Protein and mRNA expressions were measured employing ELISA, qRT-PCR, immunohistochemical staining, western blot, immunofluorescence staining and flow cytometry. The apoptosis of ATDC5 cells was determined using flow cytometry. Besides, co-IP and immunofluorescence co-localization were employed to assess the binding of ENTR1 to PTPN13.
RESULTS: ENTR1 was notably downregulated in the cartilage tissues of patients with OA and rats with DMM-induced OA, and in IL-1β-stimulated ATDC5 cells. ENTR1 overexpression attenuated the development of DMM-induced OA in rats via inhibiting inflammation, mitigating cartilage degradation and preventing chondrocyte apoptosis In the cell model of OA, upregulation of ENTR1 alleviated apoptosis, and mitigated inflammation and ECM degradation. Moreover, we found that ENTR1 overexpression decreased the FAS surface level in IL-1β-induced ATDC5 cells by binding PTPN13. Besides, ENTR1 silencing promoted apoptosis and inflammation by increasing the FAS surface level in IL-1β-induced ATDC5 cells.
CONCLUSION: ENTR1 could ameliorate OA progression through decreasing FAS surface level by binding PTPN13.
METHODS: We established OA rat model via the destabilization of the medial meniscus (DMM) surgery and OA cell model via IL-1β-stimulated ATDC5 cells. HE and safranin O/fast green staining were employed to assess the pathological changes of cartilage tissues in rats. Moreover, TUNEL staining was applied to examine chondrocyte apoptosis in rat cartilage tissues. Protein and mRNA expressions were measured employing ELISA, qRT-PCR, immunohistochemical staining, western blot, immunofluorescence staining and flow cytometry. The apoptosis of ATDC5 cells was determined using flow cytometry. Besides, co-IP and immunofluorescence co-localization were employed to assess the binding of ENTR1 to PTPN13.
RESULTS: ENTR1 was notably downregulated in the cartilage tissues of patients with OA and rats with DMM-induced OA, and in IL-1β-stimulated ATDC5 cells. ENTR1 overexpression attenuated the development of DMM-induced OA in rats via inhibiting inflammation, mitigating cartilage degradation and preventing chondrocyte apoptosis In the cell model of OA, upregulation of ENTR1 alleviated apoptosis, and mitigated inflammation and ECM degradation. Moreover, we found that ENTR1 overexpression decreased the FAS surface level in IL-1β-induced ATDC5 cells by binding PTPN13. Besides, ENTR1 silencing promoted apoptosis and inflammation by increasing the FAS surface level in IL-1β-induced ATDC5 cells.
CONCLUSION: ENTR1 could ameliorate OA progression through decreasing FAS surface level by binding PTPN13.