Journal
JOURNAL OF CELL BIOLOGY
Volume 179, Issue 5, Pages 999-1009Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.200707150
Keywords
-
Categories
Funding
- NCI NIH HHS [P01 CA041086] Funding Source: Medline
- NIGMS NIH HHS [T32 GM007388, R01 GM059383] Funding Source: Medline
Ask authors/readers for more resources
Diastrophic dysplasia sulfate transporter ( DTDST) is a sulfate/ chloride antiporter whose function is impaired in several human chondrodysplasias. We show that DTDST is upregulated by dexamethasone stimulation of HT1080. fibrosarcoma cells and is required for. fibronectin ( FN) extracellular matrix deposition by these cells. DTDST imports sulfate for the modi. cation of glycosaminoglycans. We find that N- sulfation of these chains is important for FN matrix assembly and that sulfation of cell surface proteoglycans is reduced in the absence of DTDST. Of the candidate HT1080 cell surface proteoglycans, only loss of syndecan- 2 compromises FN assembly, as shown by syndecan- 2 small interfering RNA knockdown. DTDST is both necessary and suf. cient to induce FN matrix assembly in HT1080 cells. Knockdown of DTDST ablates FN matrix, whereas its overexpression increases assembly without dexamethasone stimulation. These results identify a previously unrecognized regulatory pathway for matrix assembly via modulation of a sulfate transporter and proteoglycan sulfation. These data raise the possibility that FN assembly defects contribute to chondrodysplasias.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available