A significant part of macrophage-derived growth factor consists of at least two forms of PDGF

Shimokado, Kentaro; Raines, Elaine W.; Madtes, David K.; Barrett, Thomas B.; Benditt, Earl P.; Ross, Russell

doi:10.1016/0092-8674(85)90033-9

Cited by 673 publications

(215 citation statements)

References 46 publications

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“…tinct growth factors that bind to heparin. One of these HBGFs elutes from immobilized heparin with 0.5 M NaCI and can be shown to be PDGFlike, confirming earlier reports of macrophagederived PDGF (Shimokado et al, 1985;Mornex et al, 1986). The evidence that the HBGF eluting at 0.5 M NaCI is PDGF-like includes coelution with human PDGF on immobilized heparin columns, neutralization of growth activity by antisera that neutralize PDGF, inactivation by disulfide reducing agents, and resistance to heating at 100°C.…”

Section: Introductionsupporting

confidence: 72%

“…It is not neutralized by anti-PDGF antisera, suggesting that it is not a PDGF-like growth factor. At 1-2 d in culture, it is difficult to ascertain the cellular origin of these two HBGFs because at this point mononuclear cell preparations are contaminated by other cells such as platelets, which are known producers of growth factors such as PDGF (Shimokado et aL, 1985;Mornex et al, 1986) and platelet-derived endothelial cell growth factor (PD-ECGF) (Ishikawa et al, 1989). In general, there is about one to five times more PDGF compared with the higher affinity-binding HBGF in the conditioned medium of 1-2-d-old mononuclear cells.…”

Section: Introductionmentioning

confidence: 99%

“…Macrophages produce many growth factors, possibly more than any other cell type. Among the well-characterized macrophage-derived growth factors are platelet-derived growth factor (PDGF) (Shimokado et al, 1985;Mornex et al, 1986), basic fibroblast growth factor (bFGF) (Baird et al, 1985), transforming growth factoralpha (TGF-a) (Madtes et al, 1988), transforming growth factor-beta (TGF-fl) (Assoian et al, 1987), interleukin-1 (IL-1) (Hazuda et al, 1988;Schmidt et al, 1984), and tumor necrosis factoralpha (TN F-a) (Leibovich et al, 1988). Additional macrophage-derived growth factors have been reported but they have yet to be fully characterized and purified (Madtes et aL, 1988;Singh et al, 1988).…”

Section: Introductionmentioning

confidence: 99%

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Isolation and characterization of a macrophage-derived heparin-binding growth factor.

1990

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Human mononuclear cells were plated in culture, and the conditioned media of these cells were analyzed by heparin-Sepharose affinity chromatography. The fractions were tested for growth factor activity as measured by the stimulation of DNA synthesis in BALB/c 3T3 cells. After 2 d in culture, two peaks of heparin-binding growth factor (HBGF) activity were detected, one eluting with 0.5 M NaCI, which could be shown to be platelet-derived growth factor (PDGF)-like, and the other eluting with 1.0 M NaCI. After 7-11 d in culture, when monocytes had clearly differentiated into macrophages, >95% of the HBGF activity in conditioned medium consisted of the 1.0 M NaCI elution peak. This activity, which was designated macrophage-derived HBGF (MD-HBGF), was found to be a cationic heat-resistant polypeptide with a molecular weight in the range of 14-25 kDa. Analysis using Western blots and specific neutralizing antisera, as well as comparative heparin affinity analysis, indicated that MD-HBGF was not identical to other heparin-binding 3T3 cell growth factors known to be produced by macrophages, such as PDGF (AB, AA, and BB forms), acidic fibroblast growth factor, and basic fibroblast growth factor. In addition to stimulating mitogenesis in 3T3 cells, MD-HBGF also stimulated the proliferation of vascular smooth muscle cells, but did not stimulate the proliferation of vascular endothelial cells.

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Section: Introductionsupporting

confidence: 72%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Isolation and characterization of a macrophage-derived heparin-binding growth factor.

1990

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“…Other studies have shown that activated human alveolar macrophage secrete PDGFs Mornex et al, 1986;Shimokado et al, 1985). Thus, postnatally, PDGF appears to be one of the factors available to the alveolar macrophage for mediating normal lung defense and lung in¯ammation .…”

Section: Discussionmentioning

confidence: 94%

Modification of PDGFα receptor expression or function alters the metastatic phenotype of 3LL cells

Fitzer‐Attas

Feigelson

et al. 1997

Oncogene

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Functional PDGFa receptors are selectively expressed on highly lung-metastasizing clones of the 3LL Lewis lung carcinoma, but not on low-mestastatic clones. The highly metastatic clones are also growth induced in vitro by PDGF and lung conditioned medium. To investigate whether modi®cation of PDGFa receptor expression or function can a ect metastatic capability, we transfected cells of a low-metastatic 3LL clone with a full length PDGFa receptor gene and cells of a highly-metastatic clone with a truncated kinase domain PDGFa receptor gene. Introduction of the full length PDGFa receptor conferred upon low-metastatic cells the ability to grow in vitro in the presence of PDGF-AA and to colonize the lung in experimental and spontaneous metastases assays. Conversely, introduction of a truncated version of the PDGFa receptor into highly metastatic cells reduced their metastatic load to control levels. Accordingly, their responses to PDGF-AA, including growth stimulation and receptor autophosphorylation, were reduced. These results demonstrate that PDGFa receptor expression and function can control the capacity of tumor cells to generate metastases in the lung. The response of this receptor to lung-derived PDGF-like factors may de®ne a paracrine mode of metastatic cell growth in the target organ.

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“…Endothelial cells (DiCorleto & Bowen-Pope, 1983) and activated macrophages (Shimokado et al, 1985;Martinet et al, 1986) are examples of normal cells that produce PDGF but do not have PDGF receptors. Though it is unlikely that the PDGF production in these cases has any autocrine function, it is possible that the factor stimulates neighbouring cells in a paracrine fashion.…”

mentioning

confidence: 99%

Structural and functional aspects of platelet-derived growth factor

Hammacher²,

Nistér³

et al. 1988

Br J Cancer

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Summary The finding that PDGF production is common in normal as well as transformed cells indicate that PDGF has a function in autocrine and paracrine stimulation of cells in several physiological and pathological conditions. The expression of mRNA for the two chains of PDGF are independently regulated. The fact that the different dimeric forms of PDGF have different functional effects, indicate that the cellular response to PDGF may be more complex than previously thought, and may involve binding to more than one receptor. The cellular effects ascribed to PDGF, growth stimulation, ruffling and chemotaxis, seems to be mainly associated with B chain containing dimers. The function of PDGF-AA remains to be elucidated.

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A significant part of macrophage-derived growth factor consists of at least two forms of PDGF

Cited by 673 publications

References 46 publications

Isolation and characterization of a macrophage-derived heparin-binding growth factor.

Isolation and characterization of a macrophage-derived heparin-binding growth factor.

Modification of PDGFα receptor expression or function alters the metastatic phenotype of 3LL cells

Structural and functional aspects of platelet-derived growth factor

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