Chondromodulin I Is Dispensable during Enchondral Ossification and Eye Development.
(2002) In Molecular and Cellular Biology 22(18). p.6627-6635- Abstract
- Chondromodulin I (chm-I), a type II transmembrane protein, is highly expressed in the avascular zones of cartilage but is downregulated in the hypertrophic region, which is invaded by blood vessels during enchondral ossification. In vitro and in vivo assays with the purified protein have shown chondrocyte-modulating and angiogenesis-inhibiting functions. To investigate chm-I function in vivo, we generated transgenic mice lacking chm-I mRNA and protein. Null mice are viable and fertile and show no morphological changes. No abnormalities in vascular invasion and cartilage development were detectable. No evidence was found for a compensating function of tendin, a recently published homologue highly expressed in tendons and also, at low... (More)
- Chondromodulin I (chm-I), a type II transmembrane protein, is highly expressed in the avascular zones of cartilage but is downregulated in the hypertrophic region, which is invaded by blood vessels during enchondral ossification. In vitro and in vivo assays with the purified protein have shown chondrocyte-modulating and angiogenesis-inhibiting functions. To investigate chm-I function in vivo, we generated transgenic mice lacking chm-I mRNA and protein. Null mice are viable and fertile and show no morphological changes. No abnormalities in vascular invasion and cartilage development were detectable. No evidence was found for a compensating function of tendin, a recently published homologue highly expressed in tendons and also, at low levels, in cartilage. Furthermore, no differences in the expression of other angiogenic or antiangiogenic factors such as transforming growth factor beta1 (TGF-beta1), TGF-beta2, TGF-beta3, fibroblast growth factor 2, and vascular endothelial growth factor were found. The surprising lack of phenotype in the chm-I-deficient mice suggests either a different function for chm-I in vivo than has been proposed or compensatory changes in uninvestigated angiogenic or angiogenesis-inhibiting factors. Further analysis using double-knockout technology will be necessary to analyze the function of chm-I in the complex process of enchondral ossification. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/110052
- author
- Brandau, Oliver LU ; Aszodi, Attila LU ; Hunziker, Ernst B. ; Neame, Peter J. ; Vestweber, Dietmar and Fässler, Reinhard LU
- organization
- publishing date
- 2002
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Molecular and Cellular Biology
- volume
- 22
- issue
- 18
- pages
- 6627 - 6635
- publisher
- American Society for Microbiology
- external identifiers
-
- pmid:12192060
- wos:000177642900029
- scopus:0036724205
- ISSN
- 0270-7306
- DOI
- 10.1128/MCB.22.18.6627-6635.2002
- language
- English
- LU publication?
- yes
- additional info
- The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Pathology, (Lund) (013030000)
- id
- d42a1ebb-bcb4-4232-8053-2b1bd4051c56 (old id 110052)
- alternative location
- http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12192060&dopt=Abstract
- date added to LUP
- 2016-04-01 11:38:41
- date last changed
- 2022-03-12 22:33:56
@article{d42a1ebb-bcb4-4232-8053-2b1bd4051c56,
abstract = {{Chondromodulin I (chm-I), a type II transmembrane protein, is highly expressed in the avascular zones of cartilage but is downregulated in the hypertrophic region, which is invaded by blood vessels during enchondral ossification. In vitro and in vivo assays with the purified protein have shown chondrocyte-modulating and angiogenesis-inhibiting functions. To investigate chm-I function in vivo, we generated transgenic mice lacking chm-I mRNA and protein. Null mice are viable and fertile and show no morphological changes. No abnormalities in vascular invasion and cartilage development were detectable. No evidence was found for a compensating function of tendin, a recently published homologue highly expressed in tendons and also, at low levels, in cartilage. Furthermore, no differences in the expression of other angiogenic or antiangiogenic factors such as transforming growth factor beta1 (TGF-beta1), TGF-beta2, TGF-beta3, fibroblast growth factor 2, and vascular endothelial growth factor were found. The surprising lack of phenotype in the chm-I-deficient mice suggests either a different function for chm-I in vivo than has been proposed or compensatory changes in uninvestigated angiogenic or angiogenesis-inhibiting factors. Further analysis using double-knockout technology will be necessary to analyze the function of chm-I in the complex process of enchondral ossification.}},
author = {{Brandau, Oliver and Aszodi, Attila and Hunziker, Ernst B. and Neame, Peter J. and Vestweber, Dietmar and Fässler, Reinhard}},
issn = {{0270-7306}},
language = {{eng}},
number = {{18}},
pages = {{6627--6635}},
publisher = {{American Society for Microbiology}},
series = {{Molecular and Cellular Biology}},
title = {{Chondromodulin I Is Dispensable during Enchondral Ossification and Eye Development.}},
url = {{https://lup.lub.lu.se/search/files/2575774/623648.pdf}},
doi = {{10.1128/MCB.22.18.6627-6635.2002}},
volume = {{22}},
year = {{2002}},
}