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Impaired endochondral ossification and angiogenesis in mice deficient in membrane-type matrix metalloproteinase I
Abstract
Membrane-type matrix metalloproteinase I (MT1-MMP)-deficient mice were found to have severe defects in skeletal development and angiogenesis. The craniofacial, axial, and appendicular skeletons were severely affected, leading to a short and domed skull, marked deceleration of postnatal growth, and death by 3 wk of age. Shortening of bones is a consequence of decreased chondrocyte proliferation in the proliferative zone of the growth plates. Defective vascular invasion of cartilage leads to enlargement of hypertrophic zones of growth plates and delayed formation of secondary ossification centers in long bones. In an in vivo corneal angiogenesis assay, null mice did not have angiogenic response to implanted FGF-2, suggesting that the defect in angiogenesis is not restricted to cartilage alone. In tissues from null mice, activation of latent matrix metalloproteinase 2 was deficient, suggesting that MT1-MMP is essential for its activation in vivo .
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MT1-MMP activates pro-MMP2.
“MT1-MMP activates pro-MMP217,22.”
From Membrane type 1 matrix metalloproteinase promotes LDL receptor shedding and accelerates the development of atherosclerosis (2021) · cites this paper as [17]
MT1-MMP null mice die at 3-4 weeks.
“Considering that MT1-MMP null mice die at 3–4 weeks17,18”
From Membrane type 1 matrix metalloproteinase promotes LDL receptor shedding and accelerates the development of atherosclerosis (2021) · cites this paper as [17]
Mmp14 haploinsufficient (Mmp14+/−) mice do not display gross postnatal phenotypes.
“Mmp14 haploinsufficient (Mmp14+/−) mice, which do not display gross postnatal phenotypes24–26.”
From MT1-MMP inhibition rejuvenates ageing brain and rescues cognitive deficits in obesity (2025) · cites this paper as [24]
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Self-citation
Metadata
- Authors
- Zhou, Z., Apte, S. S., Soininen, R., Cao, R., Baaklini, G. Y., Rauser, R. W., Wang, J., Cao, Y., & Tryggvason, K.
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2000-03-28
- Volume
- 97
- Issue
- 8
- Pages
- 4052-4057
- ISSN
- 0027-8424
- 1091-6490
- Cited by
- 666
- References
- 0
- Language
- en
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