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Endplate chondrocytes were isolated from rats and treated with H2O2 to induce oxidative stress. The calcium deposition for matrix mineralization in the cells was examined by histological staining. The expression levels of calcification\u2010related genes in individual groups of cells were determined by quantitative real time\u2010PCR (qRT\u2010PCR). Subsequently, extracellular vesicles (EVs) were purified and characterized. The effect of treatment with H2O2 and\/or Abs on the mineralization, extracellular PPi metabolism and related gene expression were determined. Oxidative stress significantly increased the mineralization and promoted the generation of main Abs from endplate chondrocytes. Abs were effectively endocytosed by endplate chondrocytes and co\u2010localized with collagen (COL)\u2010II in the cytoplasm, which enhanced the mineralization, alkaline phosphatase (ALP), osteocalcin (OCN), Runt\u2010related transcription factor 2 (RUNX2) and COL\u2010I expression in endplate chondrocytes. Furthermore, treatment either H2O2 or Abs significantly decreased PPi, but increased Pi production and treatment with both further enhancing the changes in endplate chondrocytes. Similarly, treatment either H2O2 or Abs significantly decreased the ectonucleotide pyrophosphatase\/phosphodiesterase 1 (ENPP1), and ankylosis protein (ANK) expression and ENPP1 promoter activity, but increased the tissue\u2010nonspecific alkaline phosphatase (TNAP) expression and TNAP promoter activity in endplate chondrocytes. Oxidative stress promoted the generation of Abs, which might enhance the oxidative stress\u2010mediated mineralization in endplate chondrocytes by regulating the PPi metabolism.<\/jats:p>","DOI":"10.1111\/jcmm.14268","type":"journal-article","created":{"date-parts":[[2019,3,20]],"date-time":"2019-03-20T11:19:24Z","timestamp":1553080764000},"page":"3665-3675","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":38,"title":["Apoptotic bodies from endplate chondrocytes enhance the oxidative stress\u2010induced mineralization by regulating PPi metabolism"],"prefix":"10.1111","volume":"23","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-9194-8910","authenticated-orcid":false,"given":"Feng\u2010Lai","family":"Yuan","sequence":"first","affiliation":[{"name":"Department of Orthopaedics and Central Laboratory The Third Hospital Affiliated to Nantong University Wuxi China"},{"name":"Department of Orthopaedics and Central Laboratory The 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