ArticleHistochemistry and cell biology2003
Differential binding of platelet-derived growth factor isoforms to glycosaminoglycans.
Article in Histochemistry and cell biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 39 citations in OpenAlex.
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- Chondroitin sulfate synthase 1 enhances proliferation of glioblastoma by modulating PDGFRA stability.Oncogenesis · 2020Article
- Mechanistic and therapeutic overview of glycosaminoglycans: the unsung heroes of biomolecular signaling.Glycoconjugate journal · 2016Review
- Heparin/Heparan sulfate proteoglycans glycomic interactome in angiogenesis: biological implications and therapeutical use.Molecules (Basel, Switzerland) · 2015Review
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- Corneal myofibroblast biology and pathobiology: generation, persistence, and transparency.Experimental eye research · 2012Review
- A novel mechanism of sequestering fibroblast growth factor 2 by glypican in lipid rafts, allowing skeletal muscle differentiation.Molecular and cellular biology · 2010Article
- Stem cell paracrine actions and tissue regeneration.Regenerative medicine · 2010Review
- Exploiting Surface Plasmon Resonance (SPR) Technology for the Identification of Fibroblast Growth Factor-2 (FGF2) Antagonists Endowed with Antiangiogenic Activity.Sensors (Basel, Switzerland) · 2009Article
- Innovative techniques and applications in histochemistry and cell biology.Histochemistry and cell biology · 2003Review
- Dynamic reciprocity in the wound microenvironment.Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair SocietyReview
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The platelet-derived growth factor (PDGF) family comprises disulfide-bonded dimeric isoforms and plays a key role in the proliferation and migration of mesenchymal cells. Traditionally, it consists of homo- and heterodimers of A and B polypeptide chains that occur as long (A(L) and B(L)) or short (A(S) and B(S)) isoforms. Short isoforms lack the basic C-terminal extension that mediates binding to heparin. In the present study, we show that certain PDGF isoforms bind in a specific manner to glycosaminoglycans (GAGs). Experiments performed with wild-type and mutant Chinese hamster ovary cells deficient in the synthesis of GAGs revealed that PDGF long isoforms bind to heparan sulfate and chondroitin sulfate, while PDGF short isoforms only bind to heparan sulfate. This was confirmed by digestion of cell surface GAGs with heparitinase and chondroitinase ABC and by incubation with sodium chloride to prevent GAG sulfation. Furthermore, exogenous GAGs inhibited the binding of long isoforms to the cell membrane more efficiently than that of short isoforms. Additionally, we performed surface plasmon resonance experiments to study the inhibition of PDGF isoforms binding to low molecular weight heparin by GAGs. These experiments showed that PDGF-AA(L) and PDGF-BB(S) isoforms bound to GAGs with the highest affinity. In conclusion, PDGF activity at the cell surface may depend on the expression of various cellular GAG species.
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