Platelet factor 4 modulates the mitogenic activity of basic fibroblast growth factor.

Watson, John B.; Getzler, Sarah B.; Mosher, Deane F.

doi:10.1172/jci117316

Cited by 55 publications

(37 citation statements)

References 41 publications

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“…Platelet factor 4 (PF4) was able to compete with iodinated bFGF for binding to the ECM, histidine-rich glycoprotein (HRG) was able to both prevent bFGF from binding to the ECM and to displace it, whereas antithrombin III (ATIII) had no e ect. Second, the heparin-binding proteins thrombospondin, vitronectin and b-thromboglobulin do not modulate bFGF-induced DNA synthesis whereas PF4 and HRG do (Kireeva et al, 1997;Brown and Parish, 1994;Watson et al, 1994), correlating with their abilities to displace bFGF. These proteins (PF4 and HRG) were active in the same concentration range (75 ± 125 nM) as that of hCYR61 (75 nM) observed to displace bFGF.…”

Section: Discussionmentioning

confidence: 98%

“…The presence of heparin-binding proteins may either stimulate or inhibit the action of bFGF (Watson et al, 1994). Both PF4 and HRG have been observed to inhibit rather than stimulate bFGF-induced mitogenesis in NIH3T3 cells in a heparin-dependent manner (Brown and Parish, 1994;Watson et al, 1994).…”

Section: Discussionmentioning

confidence: 99%

“…Both PF4 and HRG have been observed to inhibit rather than stimulate bFGF-induced mitogenesis in NIH3T3 cells in a heparin-dependent manner (Brown and Parish, 1994;Watson et al, 1994). It was proposed that both proteins can act as either positive or negative regulators of FGF action: they can act positively by displacing FGF from the ECM and basement membrane and making more FGF available to responsive cells, and negatively by masking HSPGs on responsive cells and preventing FGF receptor activation (Brown and Parish, 1994).…”

Section: Discussionmentioning

confidence: 99%

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Human CYR61-mediated enhancement of bFGF-induced DNA synthesis in human umbilical vein endothelial cells

Kolesnikova

Lau

1998

Oncogene

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Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Human CYR61-mediated enhancement of bFGF-induced DNA synthesis in human umbilical vein endothelial cells

Kolesnikova

Lau

1998

Oncogene

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“…In these biologic systems, ELRϪ chemokines appear to exert a direct antiproliferative effect on endothelial cells, mediated through the CXCR3 receptor (7). In addition, they may modulate the effects of the major direct-acting vascular growth factors, such as VEGF or basic fibroblast growth factor (12). The findings of high levels of expression of the ELRϪ CXC chemokines combined with almost complete absence of the ELRϩ chemokines, as well as the presence of the CXCR3 receptor on vascular endothelial cells at the sites of blood vessel injury, suggest that the angiostatic properties of the former are likely to contribute to the development of vasculopathy in juvenile DM.…”

Section: Discussionmentioning

confidence: 99%

Association between lack of angiogenic response in muscle tissue and high expression of angiostatic ELR‐negative CXC chemokines in patients with juvenile dermatomyositis: Possible link to vasculopathy

Fall

Bove

Stringer

et al. 2005

Arthritis & Rheumatism

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Objective. To investigate the relationship between the vasculopathy of juvenile dermatomyositis (juvenile DM) and the balance between the angiostatic ELR؊ and angiogenic ELR؉ CXC chemokines in the muscle of patients with the disease.Methods. The expression of 3 ELR؊ CXC chemokines (interferon-inducible protein 10 [IP-10], monokine induced by interferon-␥, and interferon-inducible T cell ␣-chemoattractant) and 2 ELR؉ CXC chemokines was quantitated in muscle biopsy samples from 7 patients with juvenile DM and 7 healthy children, by real-time polymerase chain reaction. The findings were correlated with various histopathologic features, with particular emphasis on the degree of vasculopathy. Synovial biopsy specimens from patients with juvenile rheumatoid arthritis (JRA) were used for additional comparison.Results. The angiostatic ELR؊ chemokines were expressed at high levels, while the angiogenic ELR؉ chemokines were barely detectable, in most juvenile DM samples. This contrasted sharply with the findings in both normal muscle biopsy specimens and JRA synovial tissue specimens. The expression of the ELR؊ chemokines in juvenile DM samples correlated with the intensity of mononuclear cell infiltration. Furthermore, the juvenile DM samples with the highest degree of capillary loss had the highest levels of ELR؊ CXC chemokines. The presence of IP-10 in juvenile DM muscle specimens was confirmed by immunohistochemistry analysis. In addition, immunohistochemical staining of muscle tissue revealed that CXCR3, a receptor utilized by ELR؊ CXC chemokines, was expressed in vascular endothelial cells.Conclusion. Increased expression of the interferon-induced angiostatic ELR؊ CXC chemokines is a feature of juvenile DM that parallels the degree of vasculopathy in patients with the disease. Collectively, these findings are consistent with a model in which a subset of inflammatory cells secrete angiostatic ligands, which then contribute to a local atrophying effect on the muscle's vasculature via a receptor-mediated process.Juvenile dermatomyositis (juvenile DM) is the most common of the pediatric chronic inflammatory myopathies. Although myositis is the main clinical feature of this disease, many rheumatologists view juvenile DM as a systemic vasculopathy rather than simply an

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“…Although being structurally a chemokine, PF-4 lacks chemotactic activity on neutrophils and T cells (15,16). Apart from inducing short term responses on PMN, PF-4 is involved in long term differentiation and regulatory processes such as the control of EC and fibroblast proliferation (17)(18)(19) and the support of the survival of hemopoietic stem cells and progenitor cells (20). Moreover, PF-4 suppresses IL-2 mRNA transcription and the release of IL-2 in activated human T cells, corresponding to its inhibitory effect on T cell proliferation and release of IFN-␥ (15).…”

mentioning

confidence: 99%

Platelet Factor 4/CXCL4 Induces Phagocytosis and the Generation of Reactive Oxygen Metabolites in Mononuclear Phagocytes Independently of Gi Protein Activation or Intracellular Calcium Transients

Первушина¹,

Scheuerer²,

Reiling

et al. 2004

The Journal of Immunology

105

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Platelet factor 4 (PF-4), a platelet-derived CXC chemokine, is known to prevent human monocytes from apoptosis and to promote differentiation of these cells into HLA-DR− macrophages. In this study, we investigated the role of PF-4 in the control of acute monocyte proinflammatory responses involved in the direct combat of microbial invaders. We show that PF-4 increases monocyte phagocytosis and provokes a strong formation of oxygen radicals but lacks a chemotactic activity in these cells. Compared with FMLP, PF-4-induced oxidative burst was later in its onset but was remarkably longer in its duration (lasting for up to 60 min). Furthermore, in PF-4-prestimulated cells, FMLP- as well as RANTES-induced burst responses became synergistically enhanced. As we could show, PF-4-mediated oxidative burst in monocytes does not involve Gi proteins, elevation of intracellular free calcium concentrations, or binding to CXCR3B, a novel PF-4 receptor recently discovered on endothelial cells. Moreover, we found that PF-4 acts on macrophages in a dual manner. On the one hand, very similar to GM-CSF or M-CSF, PF-4 treatment of monocytes generates macrophages with a high capacity for unspecific phagocytosis. On the other hand, short term priming of GM-CSF-induced human macrophages with PF-4 substantially increases their capability for particle ingestion and oxidative burst. A comparable effect was also observed in murine bone marrow-derived macrophages, indicating cross-reactivity of human PF-4 between both species. Taken together, PF-4 may play a crucial role in the induction and maintenance of an unspecific immune response.

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Platelet factor 4 modulates the mitogenic activity of basic fibroblast growth factor.

Cited by 55 publications

References 41 publications

Human CYR61-mediated enhancement of bFGF-induced DNA synthesis in human umbilical vein endothelial cells

Human CYR61-mediated enhancement of bFGF-induced DNA synthesis in human umbilical vein endothelial cells

Association between lack of angiogenic response in muscle tissue and high expression of angiostatic ELR‐negative CXC chemokines in patients with juvenile dermatomyositis: Possible link to vasculopathy

Platelet Factor 4/CXCL4 Induces Phagocytosis and the Generation of Reactive Oxygen Metabolites in Mononuclear Phagocytes Independently of Gi Protein Activation or Intracellular Calcium Transients

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