Table 5.
Function of the bone ECM in osteoclasts.
| Bone ECM | Functions in osteoclasts | Mechanism | Cell/Mice model | Reference |
|---|---|---|---|---|
| TSP1 | Osteoclast differentiation and activity (+) | Decrease inducible nitric oxide synthase (iNOS) | TSP1−/− mice | (Amend et al., 2015) |
| TSP2 | Osteoclastogenesis (+) | Transactivation of NFATc1; Increase RANKL/OPG ratio |
RAW 264.7 cells | (Wang et al., 2019) |
| MGP | Osteoclast differentiation and bone resorption (−) | Suppress the nuclear translocation of NFATc1 and intracellular Ca2+ flux | MGP−/− mice | (Zhang Y. et al., 2019) |
| Type I collagen | Osteoclast formation (−) | Bind with the collagen receptor LAIR-1 | Primary BMMs | (Boraschi-Diaz et al., 2018) |
| Biglycan | Osteoclast precursors differentiation (−) | Decrease TNFα and RANKL cytokine | Biglycan Fibromodulin DKO mice | (Kram et al., 2017) |
| OPN | Osteoclast activity and sealing zone formation (+) | RGD sequence interact with αvβ3 integrin | Primary BMMs | (Singh et al., 2018) |
| BSP | Osteoclast surface, number, migration and bone resorption (+) | RGD sequence interact with αvβ3 integrin | BSP−/− mice BSP−/− preosteoclast |
(Boudiffa et al., 2010) |
| OPN and BSP | Osteoclast number and bone resorption (+) | RGD sequence interact with αvβ3 integrin | OPN BSP DKO mice | (Bouleftour et al., 2019) |
DKO, double knockout.