Distribution of PG-M/versican variants in human tissues and de novo expression of isoform V3 upon endothelial cell activation, migration, and neoangiogenesis in vitro
(2002) In Journal of Biological Chemistry 277(49). p.47626-47635- Abstract
- We have carried out a comprehensive molecular mapping of PG-M/versican isoforms V0-V3 in adult human tissues and have specifically investigated how the expression of these isoforms is regulated in endothelial cells in vitro. A survey of 21 representative tissues highlighted a prevalence of V1 mRNA, demonstrated that the relative frequency of expression was V1>V2>V3greater than or equal toV2; and showed that <15% of the tissues transcribed significant levels of all four isoforms. By employing novel and previously described anti-versican antibodies we verified a ubiquitous versican deposition in normal and tumor-associated vascular structures and disclosed differences in the glycanation profiles of versicans produced in different... (More)
- We have carried out a comprehensive molecular mapping of PG-M/versican isoforms V0-V3 in adult human tissues and have specifically investigated how the expression of these isoforms is regulated in endothelial cells in vitro. A survey of 21 representative tissues highlighted a prevalence of V1 mRNA, demonstrated that the relative frequency of expression was V1>V2>V3greater than or equal toV2; and showed that <15% of the tissues transcribed significant levels of all four isoforms. By employing novel and previously described anti-versican antibodies we verified a ubiquitous versican deposition in normal and tumor-associated vascular structures and disclosed differences in the glycanation profiles of versicans produced in different vascular beds. Resting endothelial cells isolated from different tissue sources transcribed several of the versican isoforms but consistently failed to translate these mRNAs into detectable proteoglycans. However, if stimulated with tumor necrosis factor-α or vascular endothelial growth factor, they altered their versican expression by de novo transcribing the V3 isoform and by exhibiting a moderate V1/V2 production. Induced versican synthesis and de novo V3 expression was also observed in endothelial cells elicited to migrate in a wound-healing model in vitro and in angiogenic endothelial cells forming tubule-like structures in Matrigel or fibrin clots. The results suggest that, independent of the degree of vascularization, human adult tissues show a limited expression of versican isoforms V0, V2, and V3 and that endothelial cells may contribute to the deposition of versican in vascular structures, but only following proper stimulation. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/321662
- author
- Cattaruzza, S ; Schiappacassi, M ; Ljungberg-Rose, A ; Spessotto, P ; Perissinotto, D ; Mörgelin, Matthias LU ; Mucignat, MT ; Colombatti, A and Perris, R
- organization
- publishing date
- 2002
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Journal of Biological Chemistry
- volume
- 277
- issue
- 49
- pages
- 47626 - 47635
- publisher
- American Society for Biochemistry and Molecular Biology
- external identifiers
-
- wos:000179663700103
- scopus:0346037291
- pmid:12221092
- ISSN
- 1083-351X
- DOI
- 10.1074/jbc.M206521200
- 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: Cell and Matrix Biology (LUR000002), Division of Infection Medicine (BMC) (013024020)
- id
- 92b177d8-6a3f-4a06-bf93-993a2902c636 (old id 321662)
- date added to LUP
- 2016-04-01 12:32:33
- date last changed
- 2022-01-27 06:32:59
@article{92b177d8-6a3f-4a06-bf93-993a2902c636,
abstract = {{We have carried out a comprehensive molecular mapping of PG-M/versican isoforms V0-V3 in adult human tissues and have specifically investigated how the expression of these isoforms is regulated in endothelial cells in vitro. A survey of 21 representative tissues highlighted a prevalence of V1 mRNA, demonstrated that the relative frequency of expression was V1>V2>V3greater than or equal toV2; and showed that <15% of the tissues transcribed significant levels of all four isoforms. By employing novel and previously described anti-versican antibodies we verified a ubiquitous versican deposition in normal and tumor-associated vascular structures and disclosed differences in the glycanation profiles of versicans produced in different vascular beds. Resting endothelial cells isolated from different tissue sources transcribed several of the versican isoforms but consistently failed to translate these mRNAs into detectable proteoglycans. However, if stimulated with tumor necrosis factor-α or vascular endothelial growth factor, they altered their versican expression by de novo transcribing the V3 isoform and by exhibiting a moderate V1/V2 production. Induced versican synthesis and de novo V3 expression was also observed in endothelial cells elicited to migrate in a wound-healing model in vitro and in angiogenic endothelial cells forming tubule-like structures in Matrigel or fibrin clots. The results suggest that, independent of the degree of vascularization, human adult tissues show a limited expression of versican isoforms V0, V2, and V3 and that endothelial cells may contribute to the deposition of versican in vascular structures, but only following proper stimulation.}},
author = {{Cattaruzza, S and Schiappacassi, M and Ljungberg-Rose, A and Spessotto, P and Perissinotto, D and Mörgelin, Matthias and Mucignat, MT and Colombatti, A and Perris, R}},
issn = {{1083-351X}},
language = {{eng}},
number = {{49}},
pages = {{47626--47635}},
publisher = {{American Society for Biochemistry and Molecular Biology}},
series = {{Journal of Biological Chemistry}},
title = {{Distribution of PG-M/versican variants in human tissues and de novo expression of isoform V3 upon endothelial cell activation, migration, and neoangiogenesis in vitro}},
url = {{http://dx.doi.org/10.1074/jbc.M206521200}},
doi = {{10.1074/jbc.M206521200}},
volume = {{277}},
year = {{2002}},
}