ArticleInflammation2017
Vacuolar Protein Sorting 4B (VPS4B) Regulates Apoptosis of Chondrocytes via p38 Mitogen-Activated Protein Kinases (MAPK) in Osteoarthritis.
Article in Inflammation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 19 citations in OpenAlex.
- Long Non-coding RNA SNHG7 Suppresses Inflammation and Apoptosis of Chondrocytes Through Inactivating of p38 MAPK Signaling Pathway in Osteoarthritis.Molecular biotechnology · 2024Article
- Article
- Discovery and identification of EIF2AK2 as a direct key target of berberine for anti-inflammatory effects.Acta pharmaceutica Sinica. B · 2023Article
- The role of Vps4 in cancer development.Frontiers in oncology · 2023Review
- Expressions of cytokeratin 14 and proliferating cell nuclear antigen in the Hertwig's epithelial root sheath of a Vps4b knockout mouse.Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology · 2021Article
- Quercetin suppresses apoptosis of chondrocytes induced by IL-1β via inactivation of p38 MAPK signaling pathway.Experimental and therapeutic medicine · 2021Article
- Exosome: A New Player in Translational Nanomedicine.Journal of clinical medicine · 2020Review
- Article
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To aim of this study is to investigate the expression of VPS4B (vacuolar protein sorting 4B) in articular cartilage with osteoarthritis (OA) and to analyze the relationship between VPS4B and chondrocyte apoptosis. We established an OA rat model by the MLI (meniscal/ligamentous injury) modeling method, and we observed the expression of VPS4B in articular cartilage through immunohistochemistry and reverse transcription polymerase chain reaction (RT-PCR). Human SW1353 chondrosarcoma cells were treated with IL-1β to mimic the OA-like chondrocyte injury in vitro, and Western blot was employed to examine the IL-1β-induced expression of VPS4B, phosphorylated p38, and apoptotic markers, namely active caspase-3 and cleaved poly (ADP-ribose) polymerase (PARP). The co-localization of VPS4B and active caspase 3 was confirmed through immunofluorescence. We knocked down VPS4B expression through RNA interference. Western blot was carried out to detect the knockdown efficiency of VPS4B and evaluate its effects on IL-1β-stimulated expression of apoptotic markers and phosphorylated p38 in SW1353 cells. Annexin V/propidium iodide (PI) staining was used to detect chondrocyte apoptosis. VPS4B expression was significantly upregulated in articular cartilage of OA rat model. IL-1β stimulation increased the expression of VPS4B, apoptotic markers, and phosphorylated p38 in SW1353 cells. VPS4B co-localized with active caspase 3 in IL-1β-treated SW1353 cells. VPS4B inhibition significantly reduced IL-1β-stimulated expression of apoptotic markers and phosphorylated p38 in SW1353 cells. Moreover, flow cytometry assay demonstrated that VPS4B knockdown alleviated IL-1β-induced apoptosis. Our results suggested that VPS4B might facilitate chondrocyte apoptosis in OA via p38 MAPK signaling pathway. This study may provide a novel insight into the pathophysiology of OA and a potential therapeutic target for its treatment.
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