Altered endochondral bone development in matrix metalloproteinase 13-deficient mice

By D. Stickens, Danielle J. Behonick, N. Ortéga, B. Heyer, B. Hartenstein, Ying Yu, A. Fosang, Marina Schorpp-Kistner, P. Angel, Zena Werb. Development, 2004

635 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology, Rheumatology

View Paper: https://www.semanticscholar.org/paper/8c934e596d84600c710ea79d47c8977bfcc18fc1

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Citations in the corpus

Matrix metalloproteinases and the regulation of tissue remodelling (2007, background): “(6) expression of their endogenous protein inhibitors, such as tissue inhibitors of metalloproteinases (TIMPs) and α2-macroglobulin118, and (7) protease degradation.”
Hypertrophic chondrocytes can become osteoblasts and osteocytes in endochondral bone formation (2014, methodology): “Zerega B, Cermelli S, Bianco P, Cancedda R, Cancedda FD (1999) Parathyroid hormone [PTH(1-34)] and parathyroid hormone-related protein [PTHrP(1-34)] promote reversion of hypertrophic chondrocytes to a prehypertrophic proliferating phenotype and prevent terminal differentiation of osteoblast-like cel”
Progress in matrix metalloproteinase research. (2008, background): “…(2002) Mmp12 Reduced macrophage numbers in ligament injury Wright et al. (2006) Mmp13 Spontaneous abnormal growth plate, increased trabecular bone Stickens et al. (2004) Mmp14 Defects in skeletal development, arthritis and connective tissue disease Holmbeck et al. (1999) Timp3 Enhanced…”
Development of the endochondral skeleton. (2013, background): “Mouse knockout studies have shown that MMP13 plays a critical role in cleaving the extracellular matrix proteins within the hypertrophic cartilage and thus facilitating vascular invasion (Inada et al. 2004; Stickens et al. 2004).”
MATRIX METALLOPROTEINASE-13 DEFICIENT MICE ARE RESISTANT TO OSTEOARTHRITIC CARTILAGE EROSION BUT NOT CHONDROCYTE HYPERTROPHY OR OSTEOPHYTE DEVELOPMENT (2009, background): “As previously reported (22,23) there was expansion of the hypertrophic zone of the growth plate in young MMP-13 KO compared with WT mice, which resolved with time (data not shown).”
The control of chondrogenesis (2006, background): “MMP-13 deficiency results in significant interstitial collagen accumulation leading to the delay of endochondral ossification in the growth plate with increased length of the hypertrophic zone [Inada et al., 2004; Stickens et al., 2004].”
Extracellular matrix: a dynamic niche component during cancer progression (2012, positive): “Through direct or indirect means, the ECM regulates almost all cellular behavior and is indispensable for major developmental pro cesses (Wiseman et al., 2003; Stickens et al., 2004; Rebustini et al., 2009; Lu et al., 2011).”