Regulation of Chondrogenesis and Chondrocyte Differentiation by Stress

Center for Musculoskeletal Research, University of Rochester Medical Center, Rochester, New York 14642, USA.
Journal of Clinical Investigation (Impact Factor: 13.22). 03/2008; 118(2):429-38. DOI: 10.1172/JCI34174
Source: PubMed


Chondrogenesis and endochondral ossification are the cartilage differentiation processes that lead to skeletal formation and growth in the developing vertebrate as well as skeletal repair in the adult. The exquisite regulation of these processes, both in normal development and in pathologic situations, is impacted by a number of different types of stress. These include normal stressors such as mechanical loading and hypoxia as well pathologic stressors such as injury and/or inflammation and environmental toxins. This article provides an overview of the processes of chondrogenesis and endochondral ossification and their control at the molecular level. A summary of the influence of the most well-understood normal and pathologic stressors on the differentiation program is also presented.

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Available from: Matthew J Hilton, Feb 13, 2014
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    • "Analogous to embryonic skeletal development, periosteum-initiated fracture repair implicates endochondral and intramembranous bone formation, which proceed in a sequential and organized manner [5], [6]. While adult bone repair recapitulates some essential regulatory mechanisms that occur in early skeletal development, repair is a unique bone morphogenetic process, orchestrated by an ensemble of genes distinct from early skeletal development [7]. Due to an inability to directly target the periosteum, the molecular mechanisms and the implicated molecular pathway(s) that control the differentiation program of periosteal mesenchymal progenitor cells in bone fracture repair remains poorly understood. "
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    Full-text · Article · Jul 2014 · PLoS ONE
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    • "Mechanical signals are important for normal cartilage to maintain tissue integrity and homeostasis (61,62). Chondrocytes respond to changes in the levels of pro-inflammatory mediators and mechanical signals in OA (63,64). "
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    Full-text · Article · Jun 2014 · International Journal of Molecular Medicine
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    • "We speculate that a relatively softer scaffold than the studied collagen-I/III scaffold would enhance chondrogenic differentiation even further. Hypoxia is believed to trigger the embryonic condensation of mesenchymal cells and the activation of various transcriptional factors resulting in cartilage formation (Zuscik et al. 2008). Mature chondrocytes and MSCs express genes for αsmooth muscle actin (SMA), which plays a major role in cell cytoskeleton (Kim and Spector 2000; Kinner and Spector 2001; Ng et al. 2011). "
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    Full-text · Article · Nov 2013 · Cell and Tissue Research
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