SMOC2 inhibits calcification of osteoprogenitor and endothelial cells

Abstract : Tissue calcification is an important physiological process required for the normal structure and function of bone. However, ectopic or excessive calcification contributes to diseases such as chondrocalcinosis, to calcium deposits in the skin or to vascular calcification. SMOC2 is a member of the BM-40/osteonectin family of calcium-binding secreted matricel-lular proteins. Using osteoprogenitor MC3T3-E1 cells stably overexpressing SMOC2, we show that SMOC2 inhibits osteogenic differentiation and extracellular matrix mineralization. Stable Smoc2 knockdown in these cells had no effect on mineralization suggesting that endogenous SMOC2 is not essential for the mineralization process. Mineralization in MC3T3-E1 cells overexpressing mutant SMOC2 lacking the extracellular calcium-binding domain was significantly increased compared to cells overexpressing full length SMOC2. When SMOC2 overexpressing cells were cultured in the presence of extracellular calcium supplementation, SMOC2's inhibitory effect on calcification was rescued. Our observations were translationally validated in primary human periosteal-derived cells. Furthermore, SMOC2 was able to impair mineralization in transdifferentiated human umbilical vein endo-thelial cells. Taken together, our data indicate that SMOC2 can act as an inhibitor of mineral-ization. We propose a possible role for SMOC2 to prevent calcification disorders.
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Contributor : Frédéric Cailotto <>
Submitted on : Tuesday, November 20, 2018 - 10:59:57 AM
Last modification on : Thursday, July 11, 2019 - 2:10:08 PM

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Tine Peeters, Silvia Monteagudo, Przemko Tylzanowski, Frank Luyten, Rik Lories, et al.. SMOC2 inhibits calcification of osteoprogenitor and endothelial cells. PLoS ONE, Public Library of Science, 2018, 13 (6), pp.e0198104. ⟨10.1371/journal.pone.0198104⟩. ⟨hal-01927881⟩

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