Inhibition of mitogenic activity of PDGF, EGF, and FGF by interferon-?

Oleszak, Emilia L.

doi:10.1016/0014-4827(88)90295-9

Cited by 25 publications

(16 citation statements)

References 8 publications

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“…51 However, the ability of IFN-␥ to inhibit the mitogenic activity of regulatory growth factors PDGF, EGF, and FGF has been demonstrated in fibroblasts. 52 It has also been shown that IFN-␥ exhibits antiproliferative effects on some other cell types, such as endothelial cells and transformed cell lines. 49,53,54 Although IFN-␥ is normally associated with inflammatory processes, the present data support the notion that IFN-␥ has a dual role in that it can also inhibit processes normally associated with inflammation, such as proliferation and migration.…”

Section: Icm Abolishes Pdgf-induced Hfrpe Proliferation and Migrationmentioning

confidence: 99%

PDGF-C and -D Induced Proliferation/Migration of Human RPE Is Abolished by Inflammatory Cytokines

Li¹,

Maminishkis²,

Wang³

et al. 2007

Invest. Ophthalmol. Vis. Sci.

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These results suggest that proinflammatory cytokines in vivo can inhibit the proliferative effect of PDGF on human RPE and, at the same time, stimulate the proliferation of choroidal cells. They also suggest an important role of proinflammatory cytokines in overcoming local proliferative/wound-healing responses, thereby controlling the development of disease processes at the retina/RPE/choroid interface.

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Section: Icm Abolishes Pdgf-induced Hfrpe Proliferation and Migrationmentioning

confidence: 99%

PDGF-C and -D Induced Proliferation/Migration of Human RPE Is Abolished by Inflammatory Cytokines

Li¹,

Maminishkis²,

Wang³

et al. 2007

Invest. Ophthalmol. Vis. Sci.

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“…Several specific antiproliferative, anti-inflammatory agents, including methotrexate [73], interleukin-4 [74], immunotoxins [75, 76], interferon-g [77], 5-fluorouracil, daunorubicin and others [78], are being investigated in these models. An obvious advantage of employing cells for drug screening is their practicability and controllability.…”

Section: Application Of Pvr Models For Pharmaceutical Investigationmentioning

confidence: 99%

Animal Models of Proliferative Vitreoretinopathy and Their Use in Pharmaceutical Investigations

2018

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“…By this method, mobilization of calcium in IRB 2 and IRB 5 cells was found to be essentially normal in comparison with the BALB/c-3T3 parental line (Fig. 8) (3,13,18,20). There is controversy as to whether IFN inhibits cell growth by interfering with growth-stimulatory signaling pathways directly or rather by activation of a unique inhibitory pathway involving components not used in growth-stimulatory signaling pathways.…”

Section: Methodsmentioning

confidence: 95%

BALB/c-3T3 fibroblasts resistant to growth inhibition by beta interferon exhibit aberrant platelet-derived growth factor, epidermal growth factor, and fibroblast growth factor signal transduction.

Mundschau

Faller

1991

Mol. Cell. Biol.

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Several lines of evidence now exist to suggest an interaction between the platelet-derived growth factor (PDGF) growth-stimulatory signal transduction pathway and the beta interferon (IFN-j8) growth-inhibitory signal transduction pathway. The most direct examples are inhibition of PDGF-mediated gene induction and mitogenesis by IFN-4 and the effects of activators and inhibitors of the IFN-inducible double-stranded RNAdependent eIF2 kinase on expression of PDGF-inducible genes. To further investigate the nature of this PDGF/ IFN-, interaction, we selected BALB/c-3T3 cells for resistance to growth inhibition by IFN-, and analyzed the phenotypes of resulting clonal lines (called IRB cells) with respect to PDGF signal transduction. Although selected only for IFN resistance, the IRB cells were found to be defective for induction of growth-related genes c-fos, c-myc, and JE in response to PDGF. This block to signal transduction was not due to loss or inactivation of PDGF receptors, as immunoprecipitation of PDGF receptors with antiphosphotyrosine antibodies showed them to be present at equal levels in the BALB/c-3T3 and IRB cells and to be autophosphorylated normally in response to PDGF. Furthermore, treatment with other peptide growth factors (PDGF-AA, fibroblast growth factor, and epidermal growth factor) also failed to induce c-fos, c-myc, or JE expression in IRB cells. All of these growth factors, however, were able to induce another early growth-related gene, Egr-1. The block to signaling was not due to a defect in inositol phosphate metabolism, as PDGF treatment induced normal calcium mobilization and phosphotidylinositol-3-kinase activation in these cells. Activation of protein kinase C by phorbol esters did induce c-fos, c-myc, and JE in IRB cells, indicating that signaling pathways distal to this enzyme remained intact. We have previously shown that IFN-inducible enzyme activities, including doublestranded RNA-dependent eIF2 kinase and 2',5'-oligoadenylate synthetase, are normal in IRB cells. The finding that the induction of multiple growth-related genes by several independent growth factors is inhibited in these IFN-resistant cells suggests that there is a second messenger common to both growth factor and IFN signaling pathways and that this messenger is defective in these cells. Treatment of cultured cells with anti-interferon (IFN)antibodies has provided evidence that many cell types utilize the antiproliferative activity of IFN to inhibit their own proliferation via an autocrine IFN feedback mechanism (5, 6, 9, 18). The significance of this growth control mechanism is suggested by numerous reports that neutralization of the autocrine IFN or the spontaneous development of resistance to its antiproliferative effects can result in neoplasia or failure to differentiate, both of which may lead to malignancy (3, 9). Since the mechanism by which IFN inhibits cell growth is unknown, it remains to be established whether autocrine IFN has its effect by directly interacting with, and inhibiting, growth-stimulatory ...

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Inhibition of mitogenic activity of PDGF, EGF, and FGF by interferon-?

Cited by 25 publications

References 8 publications

PDGF-C and -D Induced Proliferation/Migration of Human RPE Is Abolished by Inflammatory Cytokines

PDGF-C and -D Induced Proliferation/Migration of Human RPE Is Abolished by Inflammatory Cytokines

Animal Models of Proliferative Vitreoretinopathy and Their Use in Pharmaceutical Investigations

BALB/c-3T3 fibroblasts resistant to growth inhibition by beta interferon exhibit aberrant platelet-derived growth factor, epidermal growth factor, and fibroblast growth factor signal transduction.

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