Parathyroid hormone stimulation of Syndecan-4 in osteoblastic cells

Raggatt, J. L., Qin, L., Cool, S. M., Nurcombe, V. and Partridge N. C. (2005). Parathyroid hormone stimulation of Syndecan-4 in osteoblastic cells. In: Journal of Bone and Mineral Research. 27th Annual Meeting of the American Society for Bone and Mineral Research, Nashville, Tennessee, U.S., (). 24-26 September, 2005.

Author Raggatt, J. L.
Qin, L.
Cool, S. M.
Nurcombe, V.
Partridge N. C.
Title of paper Parathyroid hormone stimulation of Syndecan-4 in osteoblastic cells
Conference name 27th Annual Meeting of the American Society for Bone and Mineral Research
Conference location Nashville, Tennessee, U.S.
Conference dates 24-26 September, 2005
Proceedings title Journal of Bone and Mineral Research   Check publisher's open access policy
Place of Publication Malden, MA., U.S.
Publisher American Society for Bone and Mineral Research; Blackwell Science
Publication Year 2005
ISSN 1523-4681
Volume 20
Issue Supp.
Language eng
Abstract/Summary Syndecan-4 is a membrane bound heparan sulphate proteoglycan that binds a number of growth factors, cytokines, proteases and cell adhesion molecules. The expression of the syndecan core proteins and their specific heparan sulphate attachments occurs in cell-, tissue- and developmentally specific patterns. In a screen to identify novel PTH regulated genes using cDNA microarray technology, we identified that syndecan-4 expression is increased in osteoblastic UMR-106-01 cells in response to parathyroid hormone (rPTH 1-34). Confirmation of these data using real time RT-PCR showed that steady state levels of syndecan-4 mRNA increased by 2 h, peaked at 4 h (4 fold) and had diminished by 12 h. The influence of PTH was restricted to syndecan-4 as the mRNA expression of the other members of the syndecan family were unchanged after PTH treatment of UMR 106-01 cells. The cAMP analogue 8Br-cAMP and the PKA activator PMA were used to investigate which of these classical PTH signal transduction pathways regulate expression of syndecan-4. The cAMP analogue 8Br-cAMP mimicked the PTH induction of syndecan-4 suggesting that the cAMP signal transduction pathway is utilized by PTH to regulate expression of the syndecan-4 gene. In contrast, PMA, which activates the PKC pathway, did not stimulate syndecan-4 mRNA expression. Cycloheximide did not affect expression of syndecan-4 mRNA in response to PTH treatment suggesting that the increase in steady state mRNA levels was due to transcriptional activation of the gene and did not require de novo protein synthesis. Interestingly regulation of syndecan-4 in osteoblastic cells also occurred in response to the pro-osteoclastic agents vitamin D3 and PGE2 suggesting syndecan-4 may have a broader role in bone biology. To confirm the in vivo significance of the PTH regulation of syndecan-4, 4 week old Sprague-Dawley rats were injected subcutaneously with vehicle (0.9% saline solution) or hPTH(1-38) (8 µg/100 g). The primary spongiosa was removed from the distal femur 0.5, 1, 4, or 8 h after injection and RNA harvested. A very rapid increase in syndecan-4 expression occurred at 0.5 h post injection, peaked at 2 h (10 fold) and had returned to base line by 4 h post injection. Taken together these data show that PTH can regulate the expression of syndecan-4 in osteoblastic cells and we therefore propose that syndecan-4 may act as a co-receptor for growth factors and cytokines in the anabolic bone response to PTH.
Subjects 0601 Biochemistry and Cell Biology
06 Biological Sciences
Q-Index Code EX
Q-Index Status Provisional Code
Institutional Status Unknown
Additional Notes Poster 134. Presentation Number: M490.

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Created: Wed, 03 Mar 2010, 14:29:43 EST by Therese Egan on behalf of Institute for Molecular Bioscience