ArticleInternational journal of molecular sciences2016
Hydrostatic Compress Force Enhances the Viability and Decreases the Apoptosis of Condylar Chondrocytes through Integrin-FAK-ERK/PI3K Pathway.
Article in International journal of molecular sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
- Mechanobiology of orofacial tissues: principles, mechanisms, and therapeutic applications.International journal of oral science · 2026Review
- Immuno-Mechanical Signaling Network Integration in Temporomandibular Joint Pathology: A TMID Conceptual Framework.International journal of molecular sciences · 2026Review
- Targeting mechanotransduction components as therapeutic strategies in osteoarthritis.Molecular biology reports · 2026Review
- Mechanical cues enhance chondrocyte function: Insights from mechanoreception, regulation, and biological responses.Mechanobiology in medicine · 2025Review
- The Effect of Different Saline Suspension Height on Injured Articular Cartilage During Arthroscopic Surgery.Cartilage · 2025Article
- Advancing Tissue Damage Repair in Geriatric Diseases: Prospects of Combining Stem Cell-Derived Exosomes with Hydrogels.International journal of nanomedicine · 2024Review
- Critical signaling molecules in the temporomandibular joint osteoarthritis under different magnitudes of mechanical stimulation.Frontiers in pharmacology · 2024Review
- Stiffened fibre-like microenvironment based on patterned equidistant micropillars directs chondrocyte hypertrophy.Materials today. Bio · 2023Article
- Mechanotransduction pathways in articular chondrocytes and the emerging role of estrogen receptor-α.Bone research · 2023Review
- Rapid induction and long-term self-renewal of neural crest-derived ectodermal chondrogenic cells from hPSCs.NPJ Regenerative medicine · 2022Article
- EXOC4 Promotes Diffuse-Type Gastric Cancer Metastasis via Activating FAK Signal.Molecular cancer research : MCR · 2022Article
- Osteogenesis-Inducing Chemical Cues Enhance the Mechanosensitivity of Human Mesenchymal Stem Cells for Osteogenic Differentiation on a Microtopographically Patterned Surface.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- NG2/CSPG4 regulates cartilage degeneration during TMJ osteoarthritis.Frontiers in dental medicine · 2022Article
- Mechanical Loading Disrupts Focal Adhesion Kinase Activation in Mandibular Fibrochondrocytes During Murine Temporomandibular Joint Osteoarthritis.Journal of oral and maxillofacial surgery : official journal of the American Association of Oral and Maxillofacial Surgeons · 2021Article
- [Research progress of different mechanical stimulation regulating chondrocytes metabolism].Sheng wu yi xue gong cheng xue za zhi = Journal of biomedical engineering = Shengwu yixue gongchengxue zazhi · 2020Review
- Article
- Extracellular Signal-Regulated Kinase: A Regulator of Cell Growth, Inflammation, Chondrocyte and Bone Cell Receptor-Mediated Gene Expression.International journal of molecular sciences · 2019Review
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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