Molecular cloning of gene sequences regulated by platelet-derived growth factor

Cochran, Brent; Reffel, Angela; Stiles, Charles D.

doi:10.1016/0092-8674(83)90037-5

Cited by 936 publications

(456 citation statements)

References 49 publications

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“…These results suggest that MCP-1 promotes skin tumor development mainly by recruitment of macrophages and elevation of inflammation, which is consistent with reduced papilloma development in MCP-1 Ϫ/Ϫ mice. 39 It should be noted that MCP-1 can be secreted by different cell types, such as fibroblasts, 50 macrophages, 51,52 endothelial cells, 53 and epithelial cells. 54 In our experiments, the decreased level of MCP-1 in the skin on depletion of FSP1 ϩ cells and the enhanced ability to produce MCP-1 after TPA stimulation by fibroblasts indicate that MCP-1 secreted by fibroblasts is sufficient to maintain DMBA/TPA-induced skin inflammation.…”

Section: Discussionmentioning

confidence: 99%

FSP1+ Fibroblasts Promote Skin Carcinogenesis by Maintaining MCP-1-Mediated Macrophage Infiltration and Chronic Inflammation

Zhang

Chen

Xiao

et al. 2011

The American Journal of Pathology

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Cancer development is often associated with increased fibroblast proliferation and extensive fibrosis; however, the role of fibroblasts during carcinogenesis remains largely unknown. Using the 7,12-dimethylbenz-(a)anthracene and 12-O-tetradecanoylphorbol-13-acetateinduced two-stage skin carcinogenesis model, we demonstrated here that there was a massive accumulation and proliferation of fibroblasts in the skin shortly after application of carcinogen. Selective abatement of these cells during the promotion stage drastically decreased incidence and progression of papillomas. This correlated well with reduced macrophage infiltration and impaired cytokine storm in the affected skin. 12-O-tetradecanoylphorbol-13-acetate stimulated skin fibroblasts, secreting high levels of monocyte chemotactic protein-1, and neutralization of this chemokine eliminated almost completely the fibroblast-induced chemotaxis of macrophages. These results strongly suggest that fibroblasts promote skin tumor development by producing monocyte chemotactic protein-1 and maintaining chronic inflammation.

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Section: Discussionmentioning

confidence: 99%

FSP1+ Fibroblasts Promote Skin Carcinogenesis by Maintaining MCP-1-Mediated Macrophage Infiltration and Chronic Inflammation

Zhang

Chen

Xiao

et al. 2011

The American Journal of Pathology

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“…8 MCP-1 (CCL2), a potent monocyte attractant, is a member of the CC subfamily. 9 It was originally isolated from mouse 3T3 fibroblasts 10 and its expression can be induced by a variety of growth factors, cytokines and bacterial lipopolysaccharide. Truncation of the N-terminal of the protein leads to a loss of function, [11][12][13][14] with residues 13-35 also involved in the recognition of its receptor, CCR2.…”

mentioning

confidence: 99%

Examination of MCP-1 (CCL2) partitioning and presentation during transendothelial leukocyte migration

et al. 2003

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It is proposed that a chemokine concentration gradient promotes vectorial leukocyte migration across the vascular endothelium during inflammation. In this study, monocyte migration across a model endothelial monolayer was assessed at defined time-points after the addition of MCP-1 (CCL2). At each time-point transendothelial migration was quantified, medium from the apical and basal surface was collected for ELISA and monolayers were stained to detect both heparan sulfate and MCP-1. Statistically significant monocyte migration was observed within 60 min of chemokine addition to the basal surface of the endothelium and an asymmetric distribution of MCP-1 across the monolayer was observed at all time-points. Dual color immunofluorescence analysis demonstrated that MCP-1 was focused into heparan sulfate-containing domains on the apical surface of some of the endothelial cells. Furthermore, no uniform concentration gradient of chemokine was observed within the space between adjacent endothelial cells with apical MCP-1 application resulting in a staining pattern identical to that observed after basal application. The addition of a functional, monomeric form of MCP-1 produced a staining pattern identical to that observed using the wild-type protein, suggesting that localized chemokine oligomerization is not responsible for generating the focal chemokine distribution. Together, these data suggest that apical presentation of concentrated, chemokine-containing domains provides sufficient stimulus to promote transendothelial leukocyte migration in the absence of the formation of a formal haptotactic concentration gradient between endothelial cells.

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“…One group, the gro genes, includes JE (Cochran et al, 1983;Takehara et al, 1987), KC (Cochran et al, 1983), melanoma growth stimulating activity (MGSA)/human gro (Richmond et al, 1983(Richmond et al, , 1985Anisowicz et al, 1988;, hamster gro (Anisowicz et al, 1987), and 9E3/ CEF4 (Bedard et al, 1987;Sugano et al, 1987). Oquendo et al (1989) have discussed the close homology between these genes and pointed out that KC, MGSA/human gro, hamster gro, and 9E3/CEF4 are essentially the same gene in mouse, human, hamster, and chicken, respectively.…”

Section: Introductionmentioning

confidence: 99%

Wound-factor-induced and cell cycle phase-dependent expression of 9E3/CEF4, the avian gro gene.

et al. 1991

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The gro genes encode for secreted proteins with sequence homologies to inflammatory mediators. Little is known about the function of these proteins or their regulation. The chicken gro (9E3/CEF4) is expressed abundantly in the cells of proliferating cultures but at very low levels in confluent cultures. In vivo, this gene is expressed in connective tissue and overexpressed at sites of injury, especially in areas of neovascularization. Here we provide a bridge between these observations by examining in culture the effect on 9E3 expression and DNA synthesis induced by cell damage and by addition of factors known to be released on wounding. We mimicked wounding by scraping swaths across confluent cultures of embryonic fibroblasts and determined the time dependence of expression of 9E3 mRNA and incorporation of 3H-thymidine. We find that 9E3 is (1) transiently expressed after "wounding" or serum-stimulation; (2) expressed in a cell cycle phase-dependent manner; it is triggered during the GO-GI transition or early in G, and subsides during S-phase; and (3) stimulated to high levels by a-flbroblast growth factor (aFGF), bFGF, transforming growth factor a (TGFa), and TGF,#, to intermediate levels by platelet-derived growth factor and not stimulated by epidermal growth factor. We also find that cells that are constantly cycling do not express 9E3, indicating that they skip either the portion of the cell cycle where 9E3 is induced or that they constituitively express a repressor of transcription or an RNA-degrading enzyme. Taken together, these observations suggest that the product of this gene could play more than one role in vivo. For example, in normal tissues the 9E3 protein could be involved in the exit of cells from the resting stage, whereas during wound healing the secreted protein or its cleavage products also could play a role in angiogenesis.

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Molecular cloning of gene sequences regulated by platelet-derived growth factor

Cited by 936 publications

References 49 publications

FSP1+ Fibroblasts Promote Skin Carcinogenesis by Maintaining MCP-1-Mediated Macrophage Infiltration and Chronic Inflammation

FSP1+ Fibroblasts Promote Skin Carcinogenesis by Maintaining MCP-1-Mediated Macrophage Infiltration and Chronic Inflammation

Examination of MCP-1 (CCL2) partitioning and presentation during transendothelial leukocyte migration

Wound-factor-induced and cell cycle phase-dependent expression of 9E3/CEF4, the avian gro gene.

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