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Open AccessArticle

Hydrostatic Compress Force Enhances the Viability and Decreases the Apoptosis of Condylar Chondrocytes through Integrin-FAK-ERK/PI3K Pathway

School of Stomatology, Zhejiang Chinese Medical University, Hangzhou 310053, China
Department of Oral Implantology and Prosthetic Dentistry, Academic Centre for Dentistry Amsterdam (ACTA), VU University Amsterdam and University of Amsterdam, MOVE Research Institute, Gustav Mahlerlaan 3004, Amsterdam 1081LA, Nord-Holland, The Netherlands
Department of Orthodontics, Peking University School and Hospital of Stomatology, Beijing 100081, China
Department of Orthopaedic Surgery, the First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou 310006, China
Department of Orthodontics, Stomatology Hospital Affiliated to Zhejiang University, Hangzhou 310053, China
Authors to whom correspondence should be addressed.
Academic Editor: Ali Mobasheri
Int. J. Mol. Sci. 2016, 17(11), 1847;
Received: 29 July 2016 / Revised: 27 September 2016 / Accepted: 31 October 2016 / Published: 7 November 2016
(This article belongs to the Special Issue Apoptotic Chondrocytes and Osteoarthritis)
Reduced mechanical stimuli in many pathological cases, such as hemimastication and limited masticatory movements, can significantly affect the metabolic activity of mandibular condylar chondrocytes and the growth of mandibles. However, the molecular mechanisms for these phenomena remain unclear. In this study, we hypothesized that integrin-focal adhesion kinase (FAK)-ERK (extracellular signal–regulated kinase)/PI3K (phosphatidylinositol-3-kinase) signaling pathway mediated the cellular response of condylar chondrocytes to mechanical loading. Primary condylar chondrocytes were exposed to hydrostatic compressive forces (HCFs) of different magnitudes (0, 50, 100, 150, 200, and 250 kPa) for 2 h. We measured the viability, morphology, and apoptosis of the chondrocytes with different treatments as well as the gene, protein expression, and phosphorylation of mechanosensitivity-related molecules, such as integrin α2, integrin α5, integrin β1, FAK, ERK, and PI3K. HCFs could significantly increase the viability and surface area of condylar chondrocytes and decrease their apoptosis in a dose-dependent manner. HCF of 250 kPa resulted in a 1.51 ± 0.02-fold increase of cell viability and reduced the ratio of apoptotic cells from 18.10% ± 0.56% to 7.30% ± 1.43%. HCFs could significantly enhance the mRNA and protein expression of integrin α2, integrin α5, and integrin β1 in a dose-dependent manner, but not ERK1, ERK2, or PI3K. Instead, HCF could significantly increase phosphorylation levels of FAK, ERK1/2, and PI3K in a dose-dependent manner. Cilengitide, the potent integrin inhibitor, could dose-dependently block such effects of HCFs. HCFs enhances the viability and decreases the apoptosis of condylar chondrocytes through the integrin-FAK-ERK/PI3K pathway. View Full-Text
Keywords: integrin; FAK; ERK; PI3K; mandibular condyle; chondrocyte; apoptosis integrin; FAK; ERK; PI3K; mandibular condyle; chondrocyte; apoptosis
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MDPI and ACS Style

Ma, D.; Kou, X.; Jin, J.; Xu, T.; Wu, M.; Deng, L.; Fu, L.; Liu, Y.; Wu, G.; Lu, H. Hydrostatic Compress Force Enhances the Viability and Decreases the Apoptosis of Condylar Chondrocytes through Integrin-FAK-ERK/PI3K Pathway. Int. J. Mol. Sci. 2016, 17, 1847.

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