[1] Verma RP, Hansch C. Matrix metalloproteinases (MMPs): chemical-biological functions and (Q)SARs [J]. Bioorg Med Chem, 2007, 38(24):2223-2268. [2] Paiva KB, Granjeiro JM. Bone tissue remodeling and development: focus on matrix metalloproteinase functions [J]. Arch Biochem Biophys, 2014, 561:74-87. [3] Brinckerhoff CE, Matrisian LM. Matrix metalloproteinases: a tail of a frog that became a prince [J]. Nat Rev Nat Rev Mol Cell Biol, 2002, 3(3):207-214. [4] Krane SM, Inada M. Matrix metalloproteinases and bone [J]. Bone, 2008, 43(1):7-18. [5] Inoue K, Mikuni-Takagaki Y, Oikawa K, et al. A crucial role for matrix metalloproteinase 2 in osteocytic canalicular formation and bone metabolism [J]. J Biol Chem, 2006, 281(44):33814-33824. [6] Nyman JS, Lynch CC, Perrien DS, et al. Differential effects between the loss of MMP-2 and MMP-9 on structural and tissue-level properties of bone [J]. J Bone Miner Res, 2011, 26(6):1252-1260. [7] Mosig RA, Dowling O, DiFeo A, et al. Loss of MMP-2 disrupts skeletal and craniofacial development and results in decreased bone mineralization, joint erosion and defects in osteoblast and osteoclast growth [J]. Hum Mol Genet, 2007, 16(9):1113-1123. [8] Kennedy AM, Inada M, Krane SM, et al. MMP13 mutation causes spondyloepimetaphyseal dysplasia, Missouri type (SEMDMO) [J]. J Clin Invest, 2005, 115(10):2832-2842. [9] Song C, Li N, Hu X, et al. A de novo variant in MMP13 identified in a patient with dominant metaphyseal anadysplasia [J]. Eur J Med Genet, 2018,pii: S1769-7212(18)30150-2. [10] Stickens D, Behonick DJ, Ortega N, et al. Altered endochondral bone development in matrix metalloproteinase 13-deficient mice [J]. Development, 2004, 131(23):5883-5895. [11] Holmbeck K, Bianco P, Caterina J, et al. MT1-MMP-deficient mice develop dwarfism, osteopenia, arthritis, and connective tissue disease due to inadequate collagen turnover [J]. Cell, 1999, 99(1):81-92. [12] Holmbeck K, Bianco P, Chrysovergis K, et al. MT1-MMP-dependent, apoptotic remodeling of unmineralized cartilage: a critical process in skeletal growth [J]. J Cell Biol, 2003, 163(3):661-671. [13] Kridel SJ, Chen E, Kotra LP, et al. Substrate hydrolysis by matrix metalloproteinase-9 [J]. J Biol Chem, 2001, 276(23):20572-20578. [14] Vandooren J, Steen PEVD, Opdenakker G. Biochemistry and molecular biology of gelatinase B or matrix metalloproteinase-9 (MMP-9): The next decade [J]. Crit Rev Biochem Mol Biol, 2013, 48(3):222. [15] Reponen P, Sahlberg C, Munaut C, et al. High expression of 92-kD type Ⅳ collagenase (gelatinase B) in the osteoclast lineage during mouse development [J]. J Cell Biol, 1994, 124(6):1091-1102. [16] Lorenzo JA, Pilbeam CC, Kalinowski JF, et al. Production of both 92- and 72-kDa gelatinases by bone cells [J]. Matrix, 1992, 12(4):282. [17] Vu TH, Shipley JM, Bergers G, et al. MMP-9/gelatinase B is a key regulator of growth plate angiogenesis and apoptosis of hypertrophic chondrocytes [J]. Cell, 1998, 93(3):411-422. [18] Colnot C, Thompson Z, Miclau T, et al. Altered fracture repair in the absence of MMP9 [J]. Development, 2003, 130(17):4123. [19] 徐小淋,杨凤雪,戴红卫,等.Micro-CT活体观察大鼠牙齿移动及复发过程的实验研究[J].口腔医学研究,2015,31(12):1193-1196. [20] Tete S, Zara S, Zizzari VL, et al. Immunohistochemical analysis of matrix metalloproteinase-9, vascular endothelial growth factor, bone sialoprotein and i-nitric oxide synthase in calvaria vs. iliac crest bone grafts [J]. Clin Oral Implants Res, 2012, 23(11):1254-1260. [21] Rice DPC, Kim HJ, Thesleff I. Detection of gelatinase B expression reveals osteoclastic bone resorption as a feature of early calvarial bone development [J]. Bone, 1997, 21(6):479-486. |