VEGF promotes cartilage angiogenesis by phospho-ERK1/2 activation of Dll4 signaling in temporomandibular joint osteoarthritis caused by chronic sleep disturbance in Wistar rats
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Yabing Dong1,2,*, Gaoyi Wu3,*, Ting Zhu1,2,*, Hongyu Chen1,2, Yong Zhu1,2, Guoxiong Zhu3, Fabin Han4, Huaqiang Zhao1
1School of Stomatology, Shandong University, Wen Hua Xi Lu, Jinan City 250012, Shandong Province, China
2Shandong Provincial Key Laboratory of Oral Tissue Regeneration, Wen Hua Xi Lu, Jinan City 250012, Shandong Province, China
3Department of Stomatology, Jinan Military General Hospital, Shi Fan Lu, Jinan City 250031, Shandong Province, China
4Center for Stem Cells and Regenerative Medicine, The Affiliated Liaocheng Hospital, Taishan Medical University, 252000, Shandong Province, China
*These authors contributed equally to this work
Huaqiang Zhao, email: email@example.com
Keywords: chronic sleep disturbance, angiogenesis, TMJ-OA, VEGF
Received: November 22, 2016 Accepted: January 18, 2017 Published: January 28, 2017
Chronic sleep disturbance (CSD) has been linked to the development of temporomandibular joint osteoarthritis (TMJ-OA). While the pathogenesis of TMJ-OA is unclear, recent studies indicate that osteochondral angiogenesis is important. We developed a rat model of CSD induced TMJ-OA to investigate the changes caused by sleep disturbance and to correlate them with vascular invasion in the TMJ. We found pathological alterations and an increased microvessel density in the rat TMJ following CSD. VEGF, Dll4 and p-ERK1/2, the expression of angiogenic factors, were highly expressed in the rat mandibular condylar cartilage and their expression increased with CSD. Furthermore, we show that VEGF-induce activation of ERK1/2, which in turn, increases Dll4 expression. Together, our results suggest that CSD can cause OA-like pathological alterations in the rat TMJ by increasing angiogenesis.
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