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. Author manuscript; available in PMC: 2009 Sep 30.
Published in final edited form as: J Steroid Biochem Mol Biol. 2007 Jan 16;103(3-5):467–472. doi: 10.1016/j.jsbmb.2006.11.003

Figure 3.

Figure 3

Schematic showing the formation of MMP-3 and PKCζ-enriched matrix vesicles via genomic regulation by 1α,25(OH)2D3. Once in the matrix, 1α,25(OH)2D3 (1,25) acts directly on matrix vesicles through an ERp60 mediated pathway resulting in increased phospholipase A2 (PLA2) activity and subsequent hydrolysis of matrix vesicle phospholipids, production of lysophospholipids and arachidonic acid, and loss of matrix vesicle membrane integrity. Hydroxyapatite crystals form within the matrix vesicle during this time. Breakdown of the vesicle membrane results in release of matrix vesicle MMP-3, which then acts on the matrix to release large latent TGF-β1 from the extracellular matrix and ultimately to release active TGF-β1 from the small latent growth factor. TGF-β1 can then act back on the cell to regulate formation and release of 1α,25(OH)2D3. 1α,25(OH)2D3 can also activate plasma membrane PLA2 via ERp60, and released arachidonic acid may also participate in the activation of matrix vesicle PKC.