ArticleCell proliferation2016
Physiological oxygen tension modulates soluble growth factor profile after crosstalk between chondrocytes and osteoblasts.
Article in Cell proliferation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 21 citations in OpenAlex.
- Significantly increased bone volume in a critical-sized defect model in the rat animal model by transplantation of a stand-alone vascularized periosteal flap.European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2025Article
- Potential bioactive coating system for high-performance absorbable magnesium bone implants.Bioactive materials · 2022Review
- Osteoblasts induce glucose-derived ATP perturbations in chondrocytes through noncontact communication.Acta biochimica et biophysica Sinica · 2022Article
- Osteoblasts impair cholesterol synthesis in chondrocytes via Notch1 signalling.Cell proliferation · 2021Article
- [Research Progress in Glucose Metabolism of Chondrocytes].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2021Review
- [Research progress on osteochondral tissue engineering].Sheng wu yi xue gong cheng xue za zhi = Journal of biomedical engineering = Shengwu yixue gongchengxue zazhi · 2019Review
- Compliant substratum modulates vinculin expression in focal adhesion plaques in skeletal cells.International journal of oral science · 2019Article
- MMP-2 and Notch signal pathway regulate migration of adipose-derived stem cells and chondrocytes in co-culture systems.Cell proliferation · 2017Article
- Modulation of chondrocyte motility by tetrahedral DNA nanostructures.Cell proliferation · 2017Article
- Effect of matrix stiffness on osteoblast functionalization.Cell proliferation · 2017Article
- Angiogenesis in a 3D model containing adipose tissue stem cells and endothelial cells is mediated by canonical Wnt signaling.Bone research · 2017Article
- The fabrication of biomimetic biphasic CAN-PAC hydrogel with a seamless interfacial layer applied in osteochondral defect repair.Bone research · 2017Article
- PCL-PEG-PCL film promotes cartilage regeneration in vivo.Cell proliferation · 2016Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesPhysiological oxygen tension plays a critical role in homoeostatic maintenance and development of endochondral bone. Based on the proximity between uncalcified cartilage and subchondral bone, and microchannels that serve as a message delivery network between them, we aimed to explore the influence of low oxygen tension on soluble factor secretion in both chondrocytes and osteoblasts, after co-culture. MATERIALS AND
methodsContact co-culture was achieved for morphological observation using red fluorescent protein (RFP)-labelled chondrocytes and green fluorescent protein (GFP)-labelled osteoblasts, and non-contact co-culture achieved by transwell chambers. This was used to screen genetic variation of growth factors in hypoxia, including respective phenotypic markers, factors involving hypoxia and angiogenesis relationships, bone morphogenetic family proteins, and other general factors.
resultsWe observed a significant increase in chondrocyte size following co-culture, in both normoxia and hypoxia, but not of osteoblasts. Expression of Aggrecan in chondrocytes and alkaline phosphatase in osteoblasts was down-regulated under hypoxia following co-culture. Under hypoxia, we found that expression of hypoxia-inducible factor-1α, vascular endothelial growth factor-A/B, VE-cadherin, bone morphogenetic protein-2, and insulin-like growth factor-1 in chondrocytes, increased, but HIF-1α, platelet-derived growth factor, BMP-5/-6 and fibroblast growth factor-1 in osteoblasts, decreased.
conclusionsThese results not only indicate the importance of crosstalk between chondrocytes and osteoblasts but also improve our understanding of the mechanisms underlying homoeostatic maintenance of endochondral bone.
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