Platelet-Derived Growth Factor

Raines, Elaine W.; Bowen‐Pope, Daniel F.; Ross, Russell

doi:10.1007/978-1-4612-3210-0_5

Cited by 53 publications

(77 citation statements)

References 254 publications

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“…These studies led us to propose that PDGF-like and TGF-a/EGF-like signaling pathways play integral roles in gut and spicule formation. In mammals, PDGF acts as a mitogen in platelets, mesenchymal cells, ECM-forming cells, glial cells, and smooth muscle cells of arterial walls (see reviews by Williams, 1989;Raines et al, 1990;Pimentel, 1994). The two forms of PDGF, PDGF-A and PDGF-B, bind as a homodimer (A-A or B-B) or as a heterodimer (A-B) to the PDGF receptor.…”

mentioning

confidence: 99%

Role for platelet‐derived growth factor‐like and epidermal growth factor‐like signaling pathways in gastrulation and spiculogenesis in the Lytechinus sea urchin embryo

Ramachandran

Govindarajan

Seid

et al. 1995

Developmental Dynamics

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The mechanisms underlying sea urchin gastrulation and spiculogenesis have been sought for decades. We have identified two growth factor signaling pathways that are involved in these developmental events. Antibodies against mammalian platelet-derived growth factor (PDGF) receptor+ inhibited gastrulation and spiculogenesis, and antibodies against human epidermal growth factor (EGF) receptor disrupted gastrulation and spicule placement in Lytechinus pictus and L. vuriegutus embryos. Our studies suggested that the antibodies affect development by inhibiting rather than activating the signaling pathways. Polyclonal and monoclonal antibodies against the mammalian receptors recognized specifically Lytechinus proteins of the expected size of 170-180 x lo3 M,. Growth factor binding assays indicated that there are approximately 1.25 x lo4 platelet-derived growth factor-like receptors per cell at the mesenchyme blastula stage of L. pictus, and human platelet-derived growth factor bound with an apparent affinity of K, = 4.4 nM to dissociated cells at the mesenchyme blastula stage. Immunolabelling experiments showed that at the gastrula stage, the Lytechinus platelet-derived growth factor-like receptors are located on the primary mesenchyme cells, the gut, and most prominently on the secondary mesenchyme cells and the stomodeum. The epidermal growth factorlike receptors stained less intensely on the gut and primary and secondary mesenchyme cells. Both receptors are expressed on the ciliary band and the gut of the pluteus larva but only the PDGF-like receptor is expressed on the primary mesenchyme cells. Pulse studies showed that the embryos are sensitive to the platelet-derived growth factor receptor$ and epidermal growth factor receptor antibodies from the blastula to sometime between the mesenchyme blastula and midgastrula stages. We show that antibodies enter the blastocoel as late as the gastrula stage. Our results suggest that platelet-derived growth factor-like and epidermal growth factor-like signaling pathways are involved in the early differentiation and morphogenesis of the sea urchin gut and spicules.

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mentioning

confidence: 99%

Role for platelet‐derived growth factor‐like and epidermal growth factor‐like signaling pathways in gastrulation and spiculogenesis in the Lytechinus sea urchin embryo

Ramachandran

Govindarajan

Seid

et al. 1995

Developmental Dynamics

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“…More than half of the clones contained PTK sequences including IFGIR. which has been previously identified in these cells, and two novel receptors which have not been identified in lymphocytes, fik-2R and PDGFR-/1 PDGFR has been previously found to be expressed on cells o'( mesenchymal origin, where it mediates a potent mitogenic response upon ligation with ligand PDGF [6][7][8]. Such ligand binding triggers PTK activity of the PDGF receptor, an event which is essential for signal transduction [9,12,13].…”

Section: Discussionmentioning

confidence: 99%

“…PDGF is a potent mitogen for cells of mesenchymal origin belonging to an expanding family of growth factors whose high-affinity binding to their protein tyrosine kinase receptors induces their activation [6,7]. The protein tyrosine kinase activity of the FDGFR is essential for signal transduction [8.9] and autophosphorylation of the receptor results in the Correspondence: DrChaim M. Roifman, Division oflmmunology/ .Mlergy, The Hospital Tor Sick Children, 555 University Ave., Toronto, ON M5G 1X8, Canada.…”

Section: Introductionmentioning

confidence: 99%

Functional platelet-derived growth factor-beta (PDGF-β) receptor expressed on early B-lineage precursor cells

Trink

Wang

Shahar

et al. 1995

Clinical and Experimental Immunology

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SUMMARYGrowth and maturation of B lymphocytes from stem cells require a series of complex processes that are dependent at least in part on growth factors. Uncontrolled expression of receptors from these early growth factors may contribute to a leukuemogenesis of such early B cell progenitors. We show here that early pre-pre-B cells, but not mature B cells, express the PDGF receptor-beta (PDGFR-/5). These receptors contain a protein tyrosine kinase domain which is activated upon ligation with PDGF in pre-pre-B cells. Further, pre-pre-B leukaemia cells seem to express more PDGFR-/3 compared with their normal counterparts, suggesting a role for these receptors in growth promotion of leukaemia cells.

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“…This functional form is intuitively sensible, but is also derived from a theoretical analysis of cell-surface receptor binding dynamics in fibroblastic cell-growth-factor interactions (Olsen et al, 1995;Raines et al;Sherratt et al, 1993).…”

Section: Mathematical Modellingmentioning

confidence: 99%

“…Pathogenic stimuli could also be related to cellular signals that either effectively enhance K~, perhaps by up-regulating ligand receptor expression in fibroblastic cells, or that deplete growth-factor inactivation sites in the extracellular milieu (Clark, 1991). There are also other possibilities, such as excessive supplies of activated growth factors or activation signals, or up-regulated binding protein levels which effectively prolong the efficacy of polypeptide growth factors in uivo (Bowen-Pope et aE., 1984;Raines et al, 1990;Sprugel et al, 1987). These scenarios are all potentially testable, with the model predictions of section 3 borne in mind.…”

Section: If K E Andmentioning

confidence: 99%

A mathematical model for fibro-proliferative wound healing disorders

Olsen¹,

Sherratt

Maini³

1996

Bltn Mathcal Biology

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The normal process of dermal wound healing fails in some cases, due to fibro-proliferative disorders such as keloid and hypertrophic scars. These types of abnormal healing may be regarded as pathologically excessive responses to wounding in terms of fibroblastic cell profiles and their inflammatory growth-factor mediators. Biologically, these conditions are poorly understood and current medical treatments are thus unreliable.In this paper, the authors apply an existing deterministic mathematical model for fibroplasia and wound contraction in adult mammalian dermis (Olsen et al., J. theor. Biol. 177, 113-128, 1995) to investigate key clinical problems concerning these healing disorders. A caricature model is proposed which retains the fundamental cellular and chemical components of the full model, in order to analyse the spatiotemporal dynamics of the initiation, progression, cessation and regression of fibro-contractive diseases in relation to normal healing. This model accounts for fibroblastic cell migration, proliferation and death and growth-factor diffusion, production by cells and tissue removal/decay.Explicit results are obtained in terms of the model processes and parameters. The rate of cellular production of the chemical is shown to be critical to the development of a stable pathological state. Further, cessation and/or regression of the disease depend on appropriate spatiotemporally varying forms for this production rate, which can be understood in terms of the bistability of the normal dermal and pathological steady states-a central property of the model, which is evident from stability and bifurcation analyses.The work predicts novel, biologically realistic and testable pathogenic and control mechanisms, the understanding of which will lead toward more effective strategies for clinical therapy of fibro-proliferative disorders.

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Platelet-Derived Growth Factor

Cited by 53 publications

References 254 publications

Role for platelet‐derived growth factor‐like and epidermal growth factor‐like signaling pathways in gastrulation and spiculogenesis in the Lytechinus sea urchin embryo

Role for platelet‐derived growth factor‐like and epidermal growth factor‐like signaling pathways in gastrulation and spiculogenesis in the Lytechinus sea urchin embryo

Functional platelet-derived growth factor-beta (PDGF-β) receptor expressed on early B-lineage precursor cells

A mathematical model for fibro-proliferative wound healing disorders

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