De-sulfation of MG-63 cell glycosaminoglycans delays in vitro osteogenesis, up-regulates cholesterol synthesis and disrupts cell cycle and the actin cytoskeleton

Kumarasuriyar, A., Lee, I., Nurcombe, V. and Cool, S. M. (2009) De-sulfation of MG-63 cell glycosaminoglycans delays in vitro osteogenesis, up-regulates cholesterol synthesis and disrupts cell cycle and the actin cytoskeleton. Journal of Cellular Physiology, 219 3: 572-583. doi:10.1002/jcp.21700


Author Kumarasuriyar, A.
Lee, I.
Nurcombe, V.
Cool, S. M.
Title De-sulfation of MG-63 cell glycosaminoglycans delays in vitro osteogenesis, up-regulates cholesterol synthesis and disrupts cell cycle and the actin cytoskeleton
Journal name Journal of Cellular Physiology   Check publisher's open access policy
ISSN 0021-9541
1097-4652
Publication date 2009-06-01
Sub-type Article (original research)
DOI 10.1002/jcp.21700
Open Access Status
Volume 219
Issue 3
Start page 572
End page 583
Total pages 12
Place of publication Hoboken, NJ, United States
Publisher John Wiley & Sons
Language eng
Subject 1314 Physiology
1308 Clinical Biochemistry
1307 Cell Biology
Abstract Glycosaminoglycan (GAG) sugars are largely responsible for the bioactivity of the proteoglycan proteins they decorate, and are particularly important for mediating the processes of cell attachment and growth factor signaling. Here, we show that chlorate-induced de-sulfation of GAGs expressed by MG-63 osteosarcoma cells results in delayed cell proliferation when the cells are exposed to chlorate for short or medium periods, but a disrupted mineralization without altered cell proliferation in response to long-term chlorate exposure. Analysis of GAG-binding growth factor activity indicated that chlorate disrupted BMP2/noggin signaling, but not FGF2 activity. Microarray analyses, which were confirmed by subsequent cell-based assays, indicated that chlorate predominantly disrupted the cell cycle and actin cytoskeleton and upregulated cholesterol synthesis, without affecting cell migration or attachment. Furthermore, we observed that disruption of the functions of the proteoglycan syndecan-4 replicated phenotypes induced by chlorate, implicating a primary role for this proteoglycan in providing bioactivity for these cells.
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collection: School of Biomedical Sciences Publications
 
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Created: Thu, 03 Sep 2009, 18:13:36 EST by Mr Andrew Martlew on behalf of School of Biomedical Sciences