Platelet-derived growth factor stimulates mouse 3T3 cell mitogenesis and leukocyte chemotaxis through different structural determinants.

Williams, Lewis T.; Antoniades, H; Goetzl, E J

doi:10.1172/jci111135

Cited by 76 publications

(25 citation statements)

References 11 publications

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“…An alternative hypothesis is that platelets and their mitogens were important in initiating migration of cells into the intima. In this regard, platelet-derived growth factor (PDGF) has been shown to be chemotactic for mesenchymal cells (4,5). The goal of this study was to determine whether, after balloon catheter denudation, inhibition of platelet adherence influenced SMCs in terms of early mRNA expression and cell proliferation.…”

Section: Introductionmentioning

confidence: 99%

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Role of platelets in smooth muscle cell proliferation and migration after vascular injury in rat carotid artery.

Fingerle

Johnson

Clowes

et al. 1989

Proc. Natl. Acad. Sci. U.S.A.

370

147

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Intimal Platelets are thought to play a major role in the formation of arterial intimal lesions (1, 2) by releasing, at sites of endothelial denudation, growth factors that stimulate smooth muscle cell (SMC) growth. Support for the role of platelets in vivo comes from the key study of Friedman et al. (3), in which these authors showed that experimentally induced intimal lesion formation in rabbit arteries was significantly inhibited by prolonged thrombocytopenia. This study was interpreted by others to suggest that platelets play an important role in the induction of SMC replication, even though no cell cycle data were presented. An alternative hypothesis is that platelets and their mitogens were important in initiating migration of cells into the intima. In this regard, platelet-derived growth factor (PDGF) has been shown to be chemotactic for mesenchymal cells (4,5). The goal of this study was to determine whether, after balloon catheter denudation, inhibition of platelet adherence influenced SMCs in terms of early mRNA expression and cell proliferation. To accomplish this, we used a single injection of a polyclonal antibody against rat platelets that prevented their adherence to the subendothelium for more than 24 hr after injury. Using this protocol, we were able to show that the absence of platelets did not affect the early proliferation of SMCs in response to injury but did inhibit formation of intimal lesions. We conclude that after balloon catheter injury platelets play a minor role in promoting medial proliferation but are important in the stimulation of SMC migration into the intima.

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Section: Introductionmentioning

confidence: 99%

mentioning

confidence: 99%

Role of platelets in smooth muscle cell proliferation and migration after vascular injury in rat carotid artery.

Fingerle

Johnson

Clowes

et al. 1989

Proc. Natl. Acad. Sci. U.S.A.

370

147

View full text Add to dashboard Cite

show abstract

“…A variety of such attractants has been described in in vitro tests for certain cells. Inflammatory cells respond to che-moattractants which would be present at wound sites, including complement peptides (9), platelet-derived peptides (10)(11)(12), and bacterial products (13)(14)(15). Endothelial cells are attracted by still other factors that are not yet well characterized (16).…”

Section: Introductionmentioning

confidence: 99%

Stimulation of granulation tissue formation by platelet-derived growth factor in normal and diabetic rats.

Grotendorst¹,

Martin²,

Pencev³

et al. 1985

J. Clin. Invest.

260

128

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Subcutaneous implantation of Hunt-Schilling wound chambers in rats induces a wound repair response causing the chamber first to fill with fluid and subsequently with connective tissue. The presence of a type I collagen gel encouraged a more rapid dispersion of cells throughout the chamber but had no effect on the rate of new collagen deposition. Addition of platelet-derived growth factor (PDGF; 50 ng/chamber) to the collagen-filled chambers caused an earlier influx of connective tissue cells, a marked increase in DNA synthesis, and a greater collagen deposition in the chamber during the first 2 wk after implantation. After 3 wk, however, the levels of collagen were similar in PDGFsupplemented and control chambers. Diabetic animals exhibited a decreased rate of repair which was restored to normal by addition of PDGF to the wound chamber. Combinations of PDGF and insulin caused an even more rapid increase in collagen deposition. These results suggest that the levels of various growth factors, particularly PDGF, may be limiting at wound sites and that supplementation of wounds with these factors can accelerate the rate of new tissue formation.

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“…Previous studies have demonstrated that human blood monocytes exhibit a chemotactic response to purified PDGF (21,22). While these studies suggested the presence of a receptor capable of binding PDGF, there is no published evidence to our knowledge to support expression of PDGF-AR or PDGF-BR in these cells.…”

Section: Discussionmentioning

confidence: 89%

Coexpression of the genes for platelet-derived growth factor B-chain receptor and macrophage colony-stimulating factor 1 receptor during monocytic differentiation.

Pantazis¹,

Kharbanda²,

Goustin³

et al. 1991

Proc. Natl. Acad. Sci. U.S.A.

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Receptors for platelet-derived growth factor (PDGF) have not been identified previously to our knowledge in human myeloid cells that also produce PDGF. Here we report that phorbol ester-treated myeloid cells differentiated along the monocytic lineage express both a full-length 5.5-kilobase (kb) mRNA and a predominant, truncated 4.6-kb mRNA coding for the PDGF B-chain receptor (PDGF-BR). PDGF-BR was identified in phorbol ester-differentiated myeloid cells by indirect immunofluorescence with an antibody specific to PDGF-BR. This anti-PDGF-BR was also used in immunoprecipitation studies to demonstrate that lysates of phorbol ester-differentiated myeloid cells contain PDGF-BR molecules of 37 kDa to 130 kDa. The results also show that the tandemly linked genes for PDGF-BR and the macrophage colony-stimulating factor 1 receptor are coexpressed in the phorbol ester-differentiated myeloid cells. Expression of these two receptor genes has not been shown previously in any cell type to our knowledge.

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Platelet-derived growth factor stimulates mouse 3T3 cell mitogenesis and leukocyte chemotaxis through different structural determinants.

Cited by 76 publications

References 11 publications

Role of platelets in smooth muscle cell proliferation and migration after vascular injury in rat carotid artery.

Role of platelets in smooth muscle cell proliferation and migration after vascular injury in rat carotid artery.

Stimulation of granulation tissue formation by platelet-derived growth factor in normal and diabetic rats.

Coexpression of the genes for platelet-derived growth factor B-chain receptor and macrophage colony-stimulating factor 1 receptor during monocytic differentiation.

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