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
(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)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/258969
- author
- 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
- organization
- publishing date
- 2005
- 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
- 2016-04-01 11:57:40
- date last changed
- 2025-04-04 13:56:36
@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}},
keywords = {{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}},
doi = {{10.1016/j.ydbio.2004.09.033}},
volume = {{277}},
year = {{2005}},
}