Cross-talk between EGFR and BMP signals regulates chondrocyte maturation during endochondral ossification.

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Abstract

[Indexed for MEDLINE] 10. Steroids. 2019 Feb;142:43-47. doi: 10.1016/j.steroids.2017.12.003. Epub 2017 Dec 9. Regulation of extracellular matrix vesicles via rapid responses to steroid hormones during endochondral bone formation. Asmussen N(1), Lin Z(2), McClure MJ(3), Schwartz Z(4), Boyan BD(5). Author information: (1)School of Integrative Life Sciences, Virginia Commonwealth University, Richmond, VA 23284, USA. (2)Department of Biomedical Engineering, School of Engineering, Virginia Commonwealth University, Richmond, VA 23284, USA; Department of Periodontics, School of Dentistry, Virginia Commonwealth University, Richmond, VA 23284, USA. (3)Department of Biomedical Engineering, School of Engineering, Virginia Commonwealth University, Richmond, VA 23284, USA. (4)Department of Biomedical Engineering, School of Engineering, Virginia Commonwealth University, Richmond, VA 23284, USA; Department of Periodontics, The University of Texas Health Science Center at San Antonio, San Antonio, TX 78229, USA. (5)Department of Biomedical Engineering, School of Engineering, Virginia Commonwealth University, Richmond, VA 23284, USA; Wallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology, Atlanta, GA 30332, USA. Electronic address: bboyan@vcu.edu. Endochondral bone formation is a precise and highly ordered process whose exact regulatory framework is still being elucidated. Multiple regulatory pathways are known to be involved. In some cases, regulation impacts gene expression, resulting in changes in chondrocyte phenotypic expression and extracellular matrix synthesis. Rapid regulatory mechanisms are also involved, resulting in release of enzymes, factors and micro RNAs stored in extracellular matrisomes called matrix vesicles. Vitamin D metabolites modulate endochondral development via both genomic and rapid membrane-associated signaling pathways. 1α,25-dihydroxyvitamin D3 [1α,25(OH)2D3] acts through the vitamin D receptor (VDR) and a membrane associated receptor, protein disulfide isomerase A3 (PDIA3). 24R,25-dihydroxyvitamin D3 [24R,25(OH)2D3] affects primarily chondrocytes in the resting zone (RC) of the growth plate, whereas 1α,25(OH)2D3 affects cells in the prehypertrophic and upper hypertrophic cell zones (GC). This includes genomically directing the cells to produce matrix vesicles with zone specific characteristics. In addition, vitamin D metabolites produced by the cells interact directly with the matrix vesicle membrane via rapid signal transduction pathways, modulating their activity in the matrix. The matrix vesicle payload is able to rapidly impact the extracellular matrix via matrix processing enzymes as well as providing a feedback mechanism to the cells themselves via the contained micro RNAs. Copyright © 2017. Published by Elsevier Inc. DOI: 10.1016/j.steroids.2017.12.003