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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

Cattaruzza, S; Schiappacassi, M; Ljungberg-Rose, A; Spessotto, P; Perissinotto, D; Mörgelin, Matthias LU ; Mucignat, MT; Colombatti, A and Perris, R (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)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Journal of Biological Chemistry
volume
277
issue
49
pages
47626 - 47635
publisher
ASBMB
external identifiers
  • wos:000179663700103
  • scopus:0346037291
ISSN
1083-351X
DOI
10.1074/jbc.M206521200
language
English
LU publication?
yes
id
92b177d8-6a3f-4a06-bf93-993a2902c636 (old id 321662)
date added to LUP
2007-08-13 14:39:00
date last changed
2017-09-24 03:47:05
@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&gt;V2&gt;V3greater than or equal toV2; and showed that &lt;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    = {ASBMB},
  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},
  volume       = {277},
  year         = {2002},
}