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Distinctive functions of membrane type 1 matrix-metalloprotease (MT1-MMP or MMP-14) in lung and submandibular gland development are independent of its role in pro-MMP-2 activation

Oblander, S A; Zhou, Z J; Galvez, B G; Starcher, B; Shannon, J M; Durbeej-Hjalt, Madeleine LU ; Arroyo, A G; Tryggvason, K and Apte, S S (2005) In Developmental Biology 277(1). p.255-269
Abstract
Membrane type 1-matrix metalloprotease (MT1-MMP or MMP-14) is a major activator of pro-MMP-2 and is essential for skeletal development. We show here that it is required for branching morphogenesis of the submandibular gland but not the lung. Instead, in the lung, it is essential for postnatal development of alveolar septae. Lung development in Mmp14-/- mice is arrested at the prealveolar stage with compensatory hyperinflation of immature saccules. Mmp2-/- mice lacked comparable defects in the lung and submandibular gland, suggesting that NIT1-MMP acts via mechanisms independent of pro-MMP-2 activation. Since the developmental defects in the lung are first manifest around the time of initial vascularization (E16.5), we investigated the... (More)
Membrane type 1-matrix metalloprotease (MT1-MMP or MMP-14) is a major activator of pro-MMP-2 and is essential for skeletal development. We show here that it is required for branching morphogenesis of the submandibular gland but not the lung. Instead, in the lung, it is essential for postnatal development of alveolar septae. Lung development in Mmp14-/- mice is arrested at the prealveolar stage with compensatory hyperinflation of immature saccules. Mmp2-/- mice lacked comparable defects in the lung and submandibular gland, suggesting that NIT1-MMP acts via mechanisms independent of pro-MMP-2 activation. Since the developmental defects in the lung are first manifest around the time of initial vascularization (E16.5), we investigated the behavior of pulmonary endothelial cells from Mmp14+/+ and Mmp14-/- mice. Endothelial cells from lungs of 1-week-old Mmp14-/- mice show reduced migration and formation of three-dimensional structures on Matrigel. Since pulmonary septal development requires capillary growth, the underlying mechanism of pulmonary hypoplasia in Mmp14-/- mice may be defective angiogenesis, supporting a model in which angiogenesis is a critical rate-limiting step for acquisition of pulmonary parenchymal mass. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
pulmonary, septation, TIMP, MMP, angiogenesis, gland, submandibular, lung, alveolization, MT1-MMP, branching morphogenesis
in
Developmental Biology
volume
277
issue
1
pages
255 - 269
publisher
Elsevier
external identifiers
  • pmid:15572153
  • wos:000225741200019
  • scopus:9644253129
ISSN
1095-564X
DOI
10.1016/j.ydbio.2004.09.033
language
English
LU publication?
yes
id
f1259ada-4125-4024-8345-1280b77b85c0 (old id 258969)
date added to LUP
2007-08-09 16:41:04
date last changed
2017-10-22 03:42:12
@article{f1259ada-4125-4024-8345-1280b77b85c0,
  abstract     = {Membrane type 1-matrix metalloprotease (MT1-MMP or MMP-14) is a major activator of pro-MMP-2 and is essential for skeletal development. We show here that it is required for branching morphogenesis of the submandibular gland but not the lung. Instead, in the lung, it is essential for postnatal development of alveolar septae. Lung development in Mmp14-/- mice is arrested at the prealveolar stage with compensatory hyperinflation of immature saccules. Mmp2-/- mice lacked comparable defects in the lung and submandibular gland, suggesting that NIT1-MMP acts via mechanisms independent of pro-MMP-2 activation. Since the developmental defects in the lung are first manifest around the time of initial vascularization (E16.5), we investigated the behavior of pulmonary endothelial cells from Mmp14+/+ and Mmp14-/- mice. Endothelial cells from lungs of 1-week-old Mmp14-/- mice show reduced migration and formation of three-dimensional structures on Matrigel. Since pulmonary septal development requires capillary growth, the underlying mechanism of pulmonary hypoplasia in Mmp14-/- mice may be defective angiogenesis, supporting a model in which angiogenesis is a critical rate-limiting step for acquisition of pulmonary parenchymal mass.},
  author       = {Oblander, S A and Zhou, Z J and Galvez, B G and Starcher, B and Shannon, J M and Durbeej-Hjalt, Madeleine and Arroyo, A G and Tryggvason, K and Apte, S S},
  issn         = {1095-564X},
  keyword      = {pulmonary,septation,TIMP,MMP,angiogenesis,gland,submandibular,lung,alveolization,MT1-MMP,branching morphogenesis},
  language     = {eng},
  number       = {1},
  pages        = {255--269},
  publisher    = {Elsevier},
  series       = {Developmental Biology},
  title        = {Distinctive functions of membrane type 1 matrix-metalloprotease (MT1-MMP or MMP-14) in lung and submandibular gland development are independent of its role in pro-MMP-2 activation},
  url          = {http://dx.doi.org/10.1016/j.ydbio.2004.09.033},
  volume       = {277},
  year         = {2005},
}