Growth factor-mediated hyper-elongation of glycosaminoglycan chains on biglycan requires transcription and translation

Sundy N.Y. Yang, Micah L. Burch, Robel Getachew, Mandy L. Ballinger, Narin Osman, Peter J. Little

Research output: Contribution to journalArticleResearchpeer-review

15 Citations (Scopus)

Abstract

The mechanism through which growth factors cause glycosaminoglycan (GAG) hyper-elongation is unclear. We have investigated the role of transcription and translation on the GAG hyper-elongation effect of plateletderived growth factor (PDGF) in human vascular smooth muscle cells (VSMCs). To determine if the response involves specific signalling pathways or the process of GAG hyper-elongation we have also investigated the effects of epidermal growth factor (EGF), transforming growth factor-β (TGF-β) and thrombin. We report that both actinomycin D and cycloheximide completely abolished the ability of PDGF to stimulate radiosulphate incorporation and GAG elongation into secreted proteoglycans, and to increase the size of xyloside GAGs. Blocking de novo protein synthesis completely prevented the action of all growth factors tested to elongate GAG chains. These results lay a foundation for further investigation into the genes and proteins implicated in this response.

Original languageEnglish
Pages (from-to)147-154
Number of pages8
JournalArchives of Physiology and Biochemistry
Volume115
Issue number3
DOIs
Publication statusPublished - Jul 2009

Keywords

  • Actinomycin D
  • Biglycan
  • Cycloheximide
  • Proteoglycans
  • Vascular smooth muscle cells

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