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Journal articles on the topic 'Fibroblast growth factors'

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Published: 4 June 2021
Last updated: 25 July 2024

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1

Thomas, Kenneth A. "Fibroblast growth factors." FASEB Journal 1, no. 6 (December 1987): 434–40. http://dx.doi.org/10.1096/fasebj.1.6.3315806.

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2

Baird, Andrew, and Patricia A. Walicke. "Fibroblast growth factors." British Medical Bulletin 45, no. 2 (1989): 438–52. http://dx.doi.org/10.1093/oxfordjournals.bmb.a072333.

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3

Mason, Ivor. "Fibroblast growth factors." Current Biology 13, no. 9 (April 2003): R346. http://dx.doi.org/10.1016/s0960-9822(03)00270-7.

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4

Cheng, Maye F., Faizah S. Abdullah, and Matthew B. Buechler. "Essential growth factor receptors for fibroblast homeostasis and activation: Fibroblast Growth Factor Receptor (FGFR), Platelet Derived Growth Factor Receptor (PDGFR), and Transforming Growth Factor β Receptor (TGFβR)." F1000Research 13 (May 21, 2024): 120. http://dx.doi.org/10.12688/f1000research.143514.2.

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Fibroblasts are cells of mesenchymal origin that are found throughout the body. While these cells have several functions, their integral roles include maintaining tissue architecture through the production of key extracellular matrix components, and participation in wound healing after injury. Fibroblasts are also key mediators in disease progression during fibrosis, cancer, and other inflammatory diseases. Under these perturbed states, fibroblasts can activate into inflammatory fibroblasts or contractile myofibroblasts. Fibroblasts require various growth factors and mitogenic molecules for survival, proliferation, and differentiation. While the activity of mitogenic growth factors on fibroblasts in vitro was characterized as early as the 1970s, the proliferation and differentiation effects of growth factors on these cells in vivo are unclear. Recent work exploring the heterogeneity of fibroblasts raises questions as to whether all fibroblast cell states exhibit the same growth factor requirements. Here, we will examine and review existing studies on the influence of fibroblast growth factor receptors (FGFRs), platelet-derived growth factor receptors (PDGFRs), and transforming growth factor β receptor (TGFβR) on fibroblast cell states.
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5

Cheng, Maye F., Faizah S. Abdullah, and Matthew B. Buechler. "Essential growth factor receptors for fibroblast homeostasis and activation." F1000Research 13 (February 19, 2024): 120. http://dx.doi.org/10.12688/f1000research.143514.1.

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Fibroblasts are cells of mesenchymal origin that are found throughout the body. While these cells have several functions, their integral roles include maintaining tissue architecture through the production of key extracellular matrix components, and participation in wound healing after injury. Fibroblasts are also key mediators in disease progression during fibrosis, cancer, and other inflammatory diseases. Under these perturbed states, fibroblasts can activate into inflammatory fibroblasts or contractile myofibroblasts. Fibroblasts require various growth factors and mitogenic molecules for survival, proliferation, and differentiation. While the activity of mitogenic growth factors on fibroblasts in vitro was characterized as early as the 1970s, the proliferation and differentiation effects of growth factors on these cells in vivo are unclear. Moreover, recent work exploring the heterogeneity of fibroblasts raises questions as to whether all fibroblast cell states exhibit the same growth factor requirements. Here, we will examine and review existing growth factors known to influence fibroblast homeostasis to begin unpacking the potential growth factors that may influence in vivo fibroblast cell states.
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6

Chen, Gregory, and Reza Forough. "Fibroblast Growth Factors, Fibroblast Growth Factor Receptors, Diseases, and Drugs." Recent Patents on Cardiovascular Drug Discovery 1, no. 2 (June 1, 2006): 211–24. http://dx.doi.org/10.2174/157489006777442478.

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7

Onoue, H., Y. Ebi, H. Nakayama, XM Ru, Y. Kitamura, and J. Fujita. "Suppressive effect of Sl/Sld mouse embryo-derived fibroblast cell lines on diffusible factor-dependent proliferation of mast cells." Blood 74, no. 5 (October 1, 1989): 1557–62. http://dx.doi.org/10.1182/blood.v74.5.1557.1557.

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Abstract Two modes of mast cell growth are present, one dependent on diffusible growth factors (interleukins [IL] 3 and 4) and another dependent on contact with fibroblasts. The 3T3 fibroblast cell lines derived from WCB6F1-+/+ mouse embryos supported the proliferation of cultured mast cells (CMC), whereas the 3T3 fibroblast cell lines from WCB6F1-Sl/Sld mouse embryos did not. To investigate the relationship between growth factor-dependent and fibroblast-dependent growths of mast cells, we cocultured CMC and 3T3 fibroblasts in the presence of diffusible growth factors. WCB6F1-+/+ mouse embryo-derived 3T3 cells did not affect the growth factor-dependent proliferation of CMC, but WCB6F1-Sl/Sld mouse embryo-derived 3T3 cells significantly suppressed the proliferation. Close cell-to-cell contact was necessary for the suppression. The NWS1 fibroblast cell line was established from the spleen cells of an adult WBB6F1-+/+ mouse. Although the NWS1 cell line had no supporting effect on the proliferation of CMC in the absence of diffusible growth factors, it did not suppress the proliferation of CMC induced by the growth factors. The present result suggests that a product of mutant Sl genes may be involved in the suppressive activity of WCB6F1-Sl/Sld mouse embryo-derived 3T3 cells.
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8

Onoue, H., Y. Ebi, H. Nakayama, XM Ru, Y. Kitamura, and J. Fujita. "Suppressive effect of Sl/Sld mouse embryo-derived fibroblast cell lines on diffusible factor-dependent proliferation of mast cells." Blood 74, no. 5 (October 1, 1989): 1557–62. http://dx.doi.org/10.1182/blood.v74.5.1557.bloodjournal7451557.

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Two modes of mast cell growth are present, one dependent on diffusible growth factors (interleukins [IL] 3 and 4) and another dependent on contact with fibroblasts. The 3T3 fibroblast cell lines derived from WCB6F1-+/+ mouse embryos supported the proliferation of cultured mast cells (CMC), whereas the 3T3 fibroblast cell lines from WCB6F1-Sl/Sld mouse embryos did not. To investigate the relationship between growth factor-dependent and fibroblast-dependent growths of mast cells, we cocultured CMC and 3T3 fibroblasts in the presence of diffusible growth factors. WCB6F1-+/+ mouse embryo-derived 3T3 cells did not affect the growth factor-dependent proliferation of CMC, but WCB6F1-Sl/Sld mouse embryo-derived 3T3 cells significantly suppressed the proliferation. Close cell-to-cell contact was necessary for the suppression. The NWS1 fibroblast cell line was established from the spleen cells of an adult WBB6F1-+/+ mouse. Although the NWS1 cell line had no supporting effect on the proliferation of CMC in the absence of diffusible growth factors, it did not suppress the proliferation of CMC induced by the growth factors. The present result suggests that a product of mutant Sl genes may be involved in the suppressive activity of WCB6F1-Sl/Sld mouse embryo-derived 3T3 cells.
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9

Metzler, Veronika Maria, Christian Pritz, Anna Riml, Angela Romani, Raphaela Tuertscher, Teresa Steinbichler, Daniel Dejaco, Herbert Riechelmann, and József Dudás. "Separation of cell survival, growth, migration, and mesenchymal transdifferentiation effects of fibroblast secretome on tumor cells of head and neck squamous cell carcinoma." Tumor Biology 39, no. 11 (November 2017): 101042831770550. http://dx.doi.org/10.1177/1010428317705507.

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Fibroblasts play a central role in tumor invasion, recurrence, and metastasis in head and neck squamous cell carcinoma. The aim of this study was to investigate the influence of tumor cell self-produced factors and paracrine fibroblast–secreted factors in comparison to indirect co-culture on cancer cell survival, growth, migration, and epithelial–mesenchymal transition using the cell lines SCC-25 and human gingival fibroblasts. Thereby, we particularly focused on the participation of the fibroblast-secreted transforming growth factor beta-1.Tumor cell self-produced factors were sufficient to ensure tumor cell survival and basic cell growth, but fibroblast-secreted paracrine factors significantly increased cell proliferation, migration, and epithelial–mesenchymal transition–related phenotype changes in tumor cells. Transforming growth factor beta-1 generated individually migrating disseminating tumor cell groups or single cells separated from the tumor cell nest, which were characterized by reduced E-cadherin expression. At the same time, transforming growth factor beta-1 inhibited tumor cell proliferation under serum-starved conditions. Neutralizing transforming growth factor beta antibody reduced the cell migration support of fibroblast-conditioned medium. Transforming growth factor beta-1 as a single factor was sufficient for generation of disseminating tumor cells from epithelial tumor cell nests, while other fibroblast paracrine factors supported tumor nest outgrowth. Different fibroblast-released factors might support tumor cell proliferation and invasion, as two separate effects.
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10

COUTTS, JACQUELINE C., and JOHN T. GALLAGHER. "Receptors for fibroblast growth factors." Immunology and Cell Biology 73, no. 6 (December 1995): 584–89. http://dx.doi.org/10.1038/icb.1995.92.

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11

Pablo, Juan L., and Geoffrey S. Pitt. "Fibroblast Growth Factor Homologous Factors." Neuroscientist 22, no. 1 (December 9, 2014): 19–25. http://dx.doi.org/10.1177/1073858414562217.

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12

van Scheltinga, A. F. T., S. C. Bakker, and R. S. Kahn. "Fibroblast Growth Factors in Schizophrenia." Schizophrenia Bulletin 36, no. 6 (May 8, 2009): 1157–66. http://dx.doi.org/10.1093/schbul/sbp033.

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13

Wellstein, Anton, and Frank Czubayko. "Inhibition of fibroblast growth factors." Breast Cancer Research and Treatment 38, no. 1 (February 1996): 109–19. http://dx.doi.org/10.1007/bf01803789.

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14

PARIS, SONIA, and JACQUES POUYSSÉGUR. "Mitogenic Effects of Fibroblast Growth Factors in Cultured Fibroblastsa." Annals of the New York Academy of Sciences 638, no. 1 The Fibroblas (December 1991): 139–48. http://dx.doi.org/10.1111/j.1749-6632.1991.tb49024.x.

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15

SASADA, REIKO, MASAHARU SENO, TATSUYA WATANABE, and KOICHI IGARASHI. "Mitogenic Effects of Fibroblast Growth Factors in Cultured Fibroblastsa." Annals of the New York Academy of Sciences 638, no. 1 The Fibroblas (December 1991): 149–60. http://dx.doi.org/10.1111/j.1749-6632.1991.tb49025.x.

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16

DIONNE, CRAIG A., MICHAEL JAYE, and JOSEPH SCHLESSINGER. "Mitogenic Effects of Fibroblast Growth Factors in Cultured Fibroblastsa." Annals of the New York Academy of Sciences 638, no. 1 The Fibroblas (December 1991): 161–66. http://dx.doi.org/10.1111/j.1749-6632.1991.tb49026.x.

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17

IMOKAWA, Genji, Yukihiro YADA, Naoko MORISAKI, and Mitsutoshi KIMURA. "Biological characterization of human fibroblast-derived mitogenic factors for human melanocytes." Biochemical Journal 330, no. 3 (March 15, 1998): 1235–39. http://dx.doi.org/10.1042/bj3301235.

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To clarify the paracrine linkage between human fibroblasts and melanocytes in cutaneous pigmentation, we studied the effects of human fibroblast-derived factors on the proliferation of human melanocytes. In medium conditioned for 4 days with human fibroblast culture, factors were produced that markedly stimulated DNA synthesis of human melanocytes. The stimulatory effect was higher in medium conditioned with fibroblasts from aged skin than in medium conditioned with fibroblasts from young skin, and was interrupted by inhibitors of tyrosine kinase, such as tyrphostin, genistein and herbimycin, but not by inhibitors of protein kinases C and A, such as H-7 and phloretin. The conditioned medium was also capable of activating mitogen-activated protein kinase of human melanocytes, with old fibroblasts being more effective than young ones. Analysis of factors released into the conditioned medium revealed that levels of hepatocyte growth factor (HGF) and stem cell factor (SCF) were increased in old-fibroblast-conditioned medium compared with young-fibroblast-conditioned medium. In contrast, levels of basic fibroblast growth factor (bFGF) were similar in both media. When the conditioned medium was treated with HGF antibody with or without SCF antibody, the increase in DNA synthesis by human melanocytes was decreased to 20% of the elevated level, whereas antibodies to bFGF had no effect. Analysis of the medium conditioned for 4 days after cytokine application demonstrated that, of the cytokines tested, interleukin 1α and tumour necrosis factor α are highly effective in stimulating HGF secretion by old fibroblasts. HGF and SCF, but not bFGF, were markedly increased in culture medium in the presence of IL-1α, and this stimulatory effect was confined to young human fibroblasts. These findings suggest that SCF and HGF derived from human fibroblasts may play a part in regulating cutaneous pigmentation during inflammation and aging.
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18

Rettig, W. J., H. P. Erickson, A. P. Albino, and P. Garin-Chesa. "Induction of human tenascin (neuronectin) by growth factors and cytokines: cell type-specific signals and signalling pathways." Journal of Cell Science 107, no. 2 (February 1, 1994): 487–97. http://dx.doi.org/10.1242/jcs.107.2.487.

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The extracellular matrix protein tenascin (TN) is expressed with precise temporo-spatial patterns during embryonic and fetal development and is induced in healing wounds, inflammatory lesions and solid tumors. These tissue patterns suggest that TN synthesis may be modulated by soluble factors present in developing tissues or released from injured, inflammatory or neoplastic cells. To characterize the extrinsic control of human TN we examined the effects of several signalling molecules on cultured neural, melanocytic and fibroblastic cells. Results obtained with alpha TN antibodies in enzyme-linked immunosorbent and immunoprecipitation assays indicate that TN expression is tightly regulated in a cell type-specific manner: (1) Primitive neuroectodermal tumor (PNET) cells grown in chemically defined, serum-free media show up to > 100-fold TN induction in response to fibroblast growth factors (aFGF, bFGF, K-FGF) and phorbol ester, independent of changes in cell proliferation or total protein synthesis; no induction is seen in PNET cultures stimulated with serum or other growth and differentiation factors. (2) Normal melanocytes, which require FGF and phorbol ester for survival in vitro, fail to express TN; however, they produce TN following oncogenic transformation. (3) Fibroblasts derived from disparate tissues differ up to 100-fold in basal TN production; for example, fetal lung fibroblasts are TNhigh, but conjunctival fibroblasts derived from the same donors and fetal leptomeningeal cells are TNlow. (4) TNlow fibroblasts treated with interleukin-1, tumor necrosis factor-alpha, and interleukin-4 show up to > 100-fold increased TN secretion and TN incorporation into their extracellular matrix. Transforming growth factor-beta, which acts as an inducer of fibronectin, collagen, and integrin-type matrix receptors, has variable effects on fibroblast TN, ranging from increased deposition in the extracellular matrix of fetal conjunctival fibroblasts to reduced secretion in newborn foreskin fibroblasts. In contrast, FGFs (which are potent fibroblast mitogens), phorbol ester, bone morphogenetic proteins, and several other factors tested produced no discernible effects on fibroblast TN expression. These findings suggest that discrete sets of extrinsic signals modify TN expression in specific cell types, with the effects of a given ligand/receptor system determined by cell type-specific signalling pathways that may be linked to unique cis-regulatory elements of the TN gene. As a result, a limited set of regulatory peptides may produce highly diversified TN distribution patterns in developing and lesional tissues.
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19

Gray, A. J., J. T. Reeves, N. K. Harrison, P. Winlove, and G. J. Laurent. "Growth factors for human fibroblasts in the solute remaining after clot formation." Journal of Cell Science 96, no. 2 (June 1, 1990): 271–74. http://dx.doi.org/10.1242/jcs.96.2.271.

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Fibroblasts adhere to, and readily grow into, fibrin clots that form as a result of the cleavage of fibrinogen by thrombin. Subsequent fibroblast replication is believed to be stimulated by mitogens released by entrapped platelets, such as platelet-derived growth factor. We suggest that the supernatant remaining after the fibrinogen-thrombin reaction could stimulate fibroblast replication, even in the absence of other blood components. To examine this hypothesis we expressed liquid from a fibrin clot and measured its mitogenic activity on human lung fibroblasts, in serum-free conditions, using a colorimetric assay based on uptake and subsequent release of Methylene Blue. The clot supernatant caused a mitogenic response of 51 +/− 6% above control and was equivalent to about half that elicited by medium containing 10% newborn calf serum. On their own, both thrombin and fibrinopeptides A and B (small molecular weight cleavage products released from fibrinogen) showed some mitogenic activity, but there was also activity in higher molecular weight cleavage products, suggesting the presence of uncharacterized mitogens. It is proposed that these agents may play important roles in wound healing and diseases associated with vascular leakage and fibrosis, by stimulating fibroblast replication.
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20

Goldsmith, K. T., R. B. Gammon, and R. I. Garver. "Modulation of bFGF in lung fibroblasts by TGF-beta and PDGF." American Journal of Physiology-Lung Cellular and Molecular Physiology 261, no. 6 (December 1, 1991): L378—L385. http://dx.doi.org/10.1152/ajplung.1991.261.6.l378.

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Growth factors produced by alveolar macrophages are thought to promote the fibroblast proliferation within interstitial spaces of fibrotic lungs. This study investigated the possibility that the macrophage-produced growth factors might modulate the expression of basic fibroblast growth factor (bFGF) by lung fibroblasts. To evaluate this question, bFGF gene expression and protein production were evaluated in normal adult human lung fibroblast cell lines. Under normal culture conditions, the fibroblasts expressed the bFGF gene as two major transcripts (7.1, 3.7 kb). The addition of fetal calf serum (FCS) to serum-starved fibroblasts caused a 5- to 10-fold increase in bFGF expression. Steady-state bFGF expression was increased 108% by platelet-derived growth factor (PDGF) and 602% by transforming growth factor-beta (TGF-beta). Insulin-like growth factor-1 had no significant effect on bFGF expression. Nuclear runoff studies demonstrated that both PDGF and TGF-beta increased the relative rates of bFGF transcription in the fibroblasts. Western blot analysis of lysates from fibroblasts treated with either PDGF or TGF-beta had no detectable increase in bFGF protein above unstimulated controls. However, the simultaneous addition of PDGF and TGF-beta, or FCS, produced a marked increase in bFGF. These experiments show that two growth factors present in the alveolar airspace compartment of fibrotic lungs can promote the expression of bFGF within lung fibroblasts.
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21

Fabisiak, J. P., M. Absher, J. N. Evans, and J. Kelley. "Spontaneous production of PDGF A-chain homodimer by rat lung fibroblasts in vitro." American Journal of Physiology-Lung Cellular and Molecular Physiology 263, no. 2 (August 1, 1992): L185—L193. http://dx.doi.org/10.1152/ajplung.1992.263.2.l185.

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Platelet-derived growth factor (PDGF) is considered a decisive mediator of fibroblast growth and phenotype within the lung. The cellular sources of PDGF within the lung remain undefined. The ability of lung fibroblasts themselves to produce PDGF in vitro was therefore investigated. Northern and Western blot analyses revealed the expression of PDGF-A mRNA and secretion of A-chain containing proteins by fibroblasts derived from adult and fetal rat lung. PDGF-A gene or protein expression were below the limits of detection in two human lung fibroblast lines examined in a similar manner. PDGF-B transcripts or proteins were not detected in any lung fibroblast line examined. Conditioned medium (CM) was collected from these same lung fibroblast lines and tested for its ability to promote cell growth using human fetal lung fibroblasts as targets. Both adult and fetal rat lung fibroblasts were found to produce a potent and efficacious stimulus for cell growth. Growth-promoting activity in rat fibroblast-derived CM functioned as a "competence" factor and was partially inhibited by anti-PDGF antibody. Thus rat lung fibroblasts in vitro produce potent growth factors of which at least one appears to be PDGF-AA. Differences in the expression of PDGF-AA between rat and human lung fibroblasts exist. Growth factor-producing fibroblasts may play a role in lung repair and remodeling through production PDGF-AA in vivo.
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22

Manetti, F., F. Corelli, and M. Botta. "Fibroblast Growth Factors and Their Inhibitors." Current Pharmaceutical Design 6, no. 18 (December 1, 2000): 1897–924. http://dx.doi.org/10.2174/1381612003398528.

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23

Baker, Kevin P., and Gerrit Los. "Targeting fibroblast growth factors in cancer." Oncotarget 4, no. 7 (May 24, 2013): 952–53. http://dx.doi.org/10.18632/oncotarget.1054.

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24

Galzie, Zoya, Anne R. Kinsella, and John A. Smith. "Fibroblast growth factors and their receptors." Biochemistry and Cell Biology 75, no. 6 (December 1, 1997): 669–85. http://dx.doi.org/10.1139/o97-091.

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Fibroblast growth factors (FGFs) represent a group of polypeptide mitogens eliciting a wide variety of responses depending upon the target cell type. The knowledge of the cell surface receptors mediating the effects of FGFs has recently expanded remarkably. The complexity of the FGF family and the FGF-induced responses is reflected in the diversity and redundancy of the FGF receptors. In this review, a number of biochemical characteristics and biological properties of the FGF family and its receptors are described and their expression both in normal tissues and in tumours is discussed. Finally we speculate on the targetting of growth inhibition agents to tumours through FGF receptors. Key words: fibroblast growth factor, FGF receptor, heparan sulphate proteoglycans, tyrosine kinase receptors, FGF in tumour diagnosis.
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25

Gnatenko, D. A., E. P. Kopantsev, and E. D. Sverdlov. "Fibroblast growth factors and pancreas organogenesis." Biochemistry (Moscow), Supplement Series B: Biomedical Chemistry 11, no. 4 (October 2017): 341–48. http://dx.doi.org/10.1134/s1990750817040023.

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26

Jane Robinson, C. "Tailoring and targeting fibroblast growth factors." Trends in Biotechnology 9, no. 1 (January 1991): 147–48. http://dx.doi.org/10.1016/0167-7799(91)90049-n.

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27

Partanen, Juha, Satu Vainikka, Jaana Korhonen, Elina Armstrong, and Kari Alitalo. "Diverse receptors for fibroblast growth factors." Progress in Growth Factor Research 4, no. 1 (January 1992): 69–83. http://dx.doi.org/10.1016/0955-2235(92)90005-3.

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28

GOSPODAROWICZ, DENIS. "Biological Activities of Fibroblast Growth Factors." Annals of the New York Academy of Sciences 638, no. 1 The Fibroblas (December 1991): 1–8. http://dx.doi.org/10.1111/j.1749-6632.1991.tb49012.x.

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29

Yamaguchi, Terry P., and Janet Rossant. "Fibroblast growth factors in mammalian development." Current Opinion in Genetics & Development 5, no. 4 (August 1995): 485–91. http://dx.doi.org/10.1016/0959-437x(95)90053-j.

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30

Suzuki, Satoshi, Yutaka Ota, Kazuo Ozawa, and Toru Imamura. "Controlling Fibroblast Growth Factors for Hair Growth Regulation." Journal of Society of Cosmetic Chemists of Japan 35, no. 3 (2001): 231–36. http://dx.doi.org/10.5107/sccj.35.3_231.

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31

De Luca, Francesco, and Jeffrey Baron. "Control of Bone Growth by Fibroblast Growth Factors." Trends in Endocrinology & Metabolism 10, no. 2 (March 1999): 61–65. http://dx.doi.org/10.1016/s1043-2760(98)00120-9.

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32

Walters, J. D., R. J. Nakkula, and P. Maney. "Modulation of Gingival Fibroblast Minocycline Accumulation by Biological Mediators." Journal of Dental Research 84, no. 4 (April 2005): 320–23. http://dx.doi.org/10.1177/154405910508400405.

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Gingival fibroblasts actively accumulate tetracyclines, thereby enhancing their redistribution from blood to gingiva. Since growth factors and pro-inflammatory cytokines regulate many fibroblast activities, they could potentially enhance fibroblast minocycline accumulation. To test this hypothesis, we treated gingival fibroblast monolayers for 1 or 6 hours with platelet-derived growth factor-BB (PDGF), fibroblast growth factor-2 (FGF), transforming growth factor-β1 (TGF), or tumor necrosis factor-α (TNF). Minocycline uptake was assayed at 37° by a fluorescence method. All 4 factors significantly enhanced minocycline uptake (P ≤ 0.008, ANOVA), primarily by increasing the affinity of transport. Treatment for 6 hours with 10 ng/mL FGF, PDGF, TGF, or TNF enhanced fibroblast minocycline uptake by 19% to 25%. Phorbol myristate acetate enhanced fibroblast minocycline uptake by 28%, suggesting that protein kinase C plays a role in up-regulating transport. These effects on transport provide a mechanism by which systemic tetracyclines could be preferentially distributed to gingival wound or inflammatory sites.
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Sieuwerts, Anieta, Joan Bolt-de Vries, Peter Bosma, Susan Swiggers, Jan Klijn, John Foekens, and John Martens. "Aging of stromal-derived human breast fibroblasts might contribute to breast cancer progression." Thrombosis and Haemostasis 89, no. 02 (2003): 393–404. http://dx.doi.org/10.1055/s-0037-1613457.

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SummaryAge is an important factor in the development and spread of breast cancer. Stromal cells also contribute to breast cancer growth and metastasis through the production of extracellular matrix (ECM) modifiers such as urokinase type plasminogen activator (uPA), its receptor (uPAR), its inhibitors (PAI-1 and PAI-2), matrix metalloproteinases (MMPs), and growth factors, including the fibroblast and insulin-like growth factors (FGF’s and IGF’s). In the present study we have investigated whether breast fibroblasts aged in vitro through passage in culture display altered levels of the plasminogen activator system and growth factors that are known to modulate that system.With real-time RT-PCR we found that during passage human breast fibroblasts, whether derived from the tumour burden or from matched adjacent normal breast tissue, exhibited a consistent increase in PAI-1 and FGF-1 and a decrease in MMP-2 mRNA expression. In addition, in 5 out of 7 fibroblast strains we observed an induction of uPA expression in combination with a reduced IGF-1 expression. Interestingly, while during aging MMP-2 protein increased in all tumour-derived fibroblast strains, these protein levels were reduced in all normal-tissue-derived fibroblasts. No other clear-cut age-dependent alterations were found in the all-together 25 factors investigated. We furthermore demonstrate in one tumour-derived fibroblast strain that the increases in uPA and PAI-1 mRNA and MMP-2 protein production are inversely related to the telomere length. Artificially increasing telomere length in this fibroblast strain by expressing human telomerase reverse transcriptase (hTERT) prevented senescence and resulted in late passage cultures with early passage uPA, PAI-1 and MMP-2 levels.Our results show that aging accompanied by telomere loss induces PAI-1 and FGF-1 mRNA expression in all breast fibroblast strains, increases uPA and decreases IGF-1 mRNA expression in a subset, and increases MMP-2 protein expression only in tumour-derived breast fibroblasts. These age-induced levels of PAI-1, FGF-1, uPA and MMP-2 in stromal breast fibroblast could contribute to breast cancer progression.
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34

Tunyogi-Csapo, Miklos, Tamas Koreny, Csaba Vermes, Jorge O. Galante, Joshua J. Jacobs, and Tibor T. Glant. "Role of fibroblasts and fibroblast-derived growth factors in periprosthetic angiogenesis." Journal of Orthopaedic Research 25, no. 10 (June 7, 2007): 1378–88. http://dx.doi.org/10.1002/jor.20449.

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35

Iwasaki, Kengo, Keiko Akazawa, Mizuki Nagata, Motohiro Komaki, Yihao Peng, Makoto Umeda, Tetsuro Watabe, and Ikuo Morita. "Angiogenic Effects of Secreted Factors from Periodontal Ligament Stem Cells." Dentistry Journal 9, no. 1 (January 15, 2021): 9. http://dx.doi.org/10.3390/dj9010009.

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Periodontal disease is a chronic inflammation of tooth-supporting tissues, and the destruction of these tissues results in tooth loss. Regeneration of periodontal tissues is the ultimate goal of periodontal treatment. We previously reported that transplantation of conditioned medium (CM) of periodontal ligament stem cells (PDLSCs) demonstrated the enhancement of periodontal tissue regeneration, compared to CM from fibroblasts (Fibroblast-CM). We hypothesized that the angiogenic effects of PDLSC-CM might participate in the enhanced wound healing of periodontal tissues. The aim of this study was to investigate the effect of PDLSC-CM on the functions of endothelial cells. PDLSCs were cultured from periodontal ligament tissues obtained from healthy volunteers. Human gingival epithelial cells, dermal fibroblasts, osteoblasts, and umbilical vein endothelial cells (HUVECs) were purchased from commercial sources. The functions of endothelial cells were examined using immunostaining of Ki67, observation of nuclear fragmentation and condensation (apoptosis), and network formation on Matrigel. Vascular endothelial cell growth factor (VEGF) level was measured using an ELISA kit. HUVECs demonstrated higher cell viability in PDLSC-CM when compared with those in Fibroblast-CM. HUVECs demonstrated a higher number of Ki67-positive cells and lower apoptosis cells in PDLSC-CM, compared to Fibroblast-CM. Additionally, HUVECs formed more capillary-like structures in PDLSC-CM than Fibroblast-CM. PDLSC-CM contained higher levels of angiogenic growth factor, VEGF, than Fibroblast-CM. Our results showed that PDLSC-CM increased cell viability, proliferation, and capillary formation of HUVECs compared to Fibroblast-CM, suggesting the angiogenic effects of PDLSC-CM, and the effect is a potential regenerative mechanism of periodontal tissues by PDLSC-CM.
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36

Burhan Rafiq, Shvan, Heshu Sulaiman Rahman, and Kawa Amin. "The Estimate of Cytokines and Fibroblast Growth Factors in Patients with Breast Cancer." Journal of Zankoy Sulaimani - Part A 22, no. 2 (December 20, 2020): 9–16. http://dx.doi.org/10.17656/jzs.10803.

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37

Zucali, J. R., H. E. Broxmeyer, M. A. Gross, and C. A. Dinarello. "Recombinant human tumor necrosis factors alpha and beta stimulate fibroblasts to produce hemopoietic growth factors in vitro." Journal of Immunology 140, no. 3 (February 1, 1988): 840–44. http://dx.doi.org/10.4049/jimmunol.140.3.840.

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Abstract The influences of TNF alpha and TNF beta were evaluated for their stimulatory and inhibitory effects on in vitro colony formation by human bone marrow granulocyte-macrophage (CFU-GM), erythroid (BFU-E), and multipotential (CFU-GEMM) progenitor cells. Both TNF alpha and TNF beta induced fibroblasts to produce stimulators of CFU-GM, BFU-E, and CFU-GEMM in a dose-dependent fashion. Similar results were seen when equivalent concentrations of TNF alpha and TNF beta were used. Prior incubation of the TNF alpha and TNF beta with their respective antibodies inactivated the ability of the TNF preparations to induce the release of granulocyte-macrophage, erythroid, and multipotential colony-stimulating activity from fibroblasts. In addition, incubation of the TNF-induced fibroblast supernatant with antibody before colony assay resulted in enhanced colony formation, suggesting that the TNF carried over into the colony assay suppressed colony formation. Additional proof of this suppression by TNF was evident when TNF was added directly to the CFU-GM, BFU-E, and CFU-GEMM colony assays. IL-1 does not appear to function as an intermediary in growth factor production by fibroblasts stimulated with TNF because antibody to IL-1 displayed no effect. Furthermore, assay of TNF-induced fibroblast supernatant was negative for IL-1. These results suggest that TNF alpha and TNF beta exert both a positive and negative influence on in vitro hemopoietic colony formation.
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Nakamura, Y., L. Tate, R. F. Ertl, M. Kawamoto, T. Mio, Y. Adachi, D. J. Romberger, et al. "Bronchial epithelial cells regulate fibroblast proliferation." American Journal of Physiology-Lung Cellular and Molecular Physiology 269, no. 3 (September 1, 1995): L377—L387. http://dx.doi.org/10.1152/ajplung.1995.269.3.l377.

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Chronic bronchitis frequently leads to irreversible airway obstruction. Alteration of airway architecture with abnormal airway connective tissue is thought to play an important role in this process. We hypothesized that the epithelial cells that line the airways modulate the development of peribronchial fibrosis and fixed airway obstruction by directing fibroblast proliferation. To assess this, we examined stimulatory activities for human lung fibroblast proliferation in bovine bronchial epithelial cell-conditioned medium. The conditioned medium stimulated the proliferation of fibroblasts in a serum-free culture system in a concentration-dependent manner. The fibroblast growth stimulatory activity was heterogenous, with molecular masses of > 50 and approximately 10 kDa. Bronchial epithelial cell-conditioned medium also contained fibroblast growth inhibitory factors, including both transforming growth factor (TGF)-beta and, based on indomethacin sensitivity, cyclooxygenase products. TGF-beta appeared to contribute to the morphological change of fibroblasts induced by the conditioned medium. Co-culture of human lung fibroblasts with bronchial epithelial cells resulted in a stimulation of fibroblast proliferation. In summary, airway epithelial cells appear to regulate fibroblast proliferation and may play a role in peribronchial fibrosis in chronic bronchitis.
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Ihn, H., K. Kikuchi, Y. Soma, S. Sato, M. Fujimoto, T. Tamaki, A. Igarashi, and K. Takehara. "The stimulatory effects of PDGF and TGF-beta 1 on dermal fibroblast attachment." Acta Dermato-Venereologica 75, no. 5 (September 1, 1995): 367–71. http://dx.doi.org/10.2340/0001555575367371.

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We investigated the effects of various growth factors (platelet-derived growth factor (PDGF), epidermal growth factor (EGF), basic fibroblast growth factor (bFGF), transforming growth factor-alpha (TGF-alpha), transforming growth factor-beta 1 (TGF-beta 1), tumor necrosis factor-alpha (TNF-alpha), keratinocyte growth factor (KGF)) on fibroblast attachment to plastic plates. It is thought that cell attachment to plastic plates in vitro may represent the step between cell migration and proliferation in vivo during wound healing. Among the growth factors examined, only PDGF and TGF-beta 1 significantly increased fibroblast attachment to both uncoated and collagen-coated plates in a concentration-dependent manner. The addition of anti-PDGF antibody abolished the enhancing effect of PDGF but not that of TGF-beta 1, suggesting that the effect of TGF-beta 1 is not through the autocrine induction of PDGF-related activities secreted by the fibroblasts themselves. These data suggest that PDGF and TGF-beta 1 regulate fibroblast attachment to the suitable environment in the process of dermal wound healing in vivo.
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40

Rogers, Mary-Louise, David A. Belford, Geoffrey L. Francis, and F. John Ballard. "Identification of fibroblast growth factors in bovine cheese whey." Journal of Dairy Research 62, no. 3 (August 1995): 501–7. http://dx.doi.org/10.1017/s0022029900031198.

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SummaryAcidic and basic fibroblast growth factors (FGF) were identified in bovine cheese whey after partial purification using a two step procedure. Cation-exchange chromatography produced a mitogen-rich extract which was loaded on to a heparin-sepharose column and eluted stepwise with 0·8, 1·2 and 2·0 M-NH4HC03. Mitogenic activity was found in all three fractions by cell growth assays using Balb/c-3T3 fibroblasts. Immunoblotting identified acidic FGF in the 1·2 M-eluate and basic FGF in the 2·0 M-eluate, but neither acidic nor basic FGF was detected in the 0·8 M-fraction. Quantitative radioreceptor assays indicated 5·8 ng of acidic FGF-like activity and 19·8 ng of basic FGF-like activity per 1 whey in the appropriate eluates. This study represents the first direct demonstration of FGF in milk.
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Korc, M., and R. Friesel. "The Role of Fibroblast Growth Factors in Tumor Growth." Current Cancer Drug Targets 9, no. 5 (August 1, 2009): 639–51. http://dx.doi.org/10.2174/156800909789057006.

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42

Bidey, SP, DJ Hill, and MC Eggo. "Growth factors and goitrogenesis." Journal of Endocrinology 160, no. 3 (March 1, 1999): 321–32. http://dx.doi.org/10.1677/joe.0.1600321.

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By combining data from studies of multinodular non-toxic goitre (MNTG) with data from rat models of goitre induction and in vitro models, a map of the growth factors involved in goitrogenesis has been constructed. We have addressed the roles of the insulin-like growth factors, transforming growth factors, fibroblast growth factors, endothelins, etc. We hypothesise that an imbalance in the interactions between the various growth factor axes exists in MNTG which favours cell replication. Thyrotrophin, although not significantly elevated in MNTG, exerts critical effects through interactions with autocrine and paracrine factors and their receptors. Expansion of the thyroidal vascular bed through angiogenesis is closely co-ordinated with follicular cell expansion and folliculoneogenesis, and while the integrated paracrine actions of fibroblast growth factors, vascular endothelial growth factor and endothelin probably play central roles, additional, as yet elusive, factors are probably involved. The combination of in vitro and in vivo approaches, designed to address specific questions, will undoubtedly continue to prove invaluable in dissecting further the complex interactions that exist between these growth factors, their binding proteins and receptors in goitrogenesis.
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Trautmann, Axel, Georg Krohne, Eva-B. Bröcker, and C. Eberhard Klein. "Human Mast Cells Augment Fibroblast Proliferation by Heterotypic Cell-Cell Adhesion and Action of IL-4." Journal of Immunology 160, no. 10 (May 15, 1998): 5053–57. http://dx.doi.org/10.4049/jimmunol.160.10.5053.

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Abstract Mast cells have been implicated in the pathogenesis of fibrosis because of their increased number in chronic inflammatory reactions. In a previous study, we had shown that human mast cells readily attach and form heterotypic cell-cell contacts when seeded on top of fibroblast monolayers. Here, we report that human mast cells stimulate fibroblast proliferation after cell-cell contact. Proliferation was measured by 5-bromo-2′-deoxyuridine or [3H]thymidine uptake of subconfluent fibroblast monolayers after attachment of mast cells that had been preincubated with mitomycin C. An 18-h coculture of the human mast cell line HMC-1 doubled proliferation of normal skin fibroblasts. Moreover, normal mast cells prepared from neonatal foreskin doubled fibroblast proliferation. The stimulatory effect was dependent on heterotypic cell-cell contact since it was not transferred by tissue culture supernatants from mast cells. We hypothesized that mast cell cytokines secreted after heterotypic cell-cell contact stimulate fibroblast proliferation. Several mast cell-derived cytokines were tested for effects on fibroblast proliferation. Only IL-4 was able to double fibroblast proliferation. Additional experiments revealed that: 1) the stimulatory effect of IL-4 as well as of the mast cell coculture could be completely abrogated by preincubation of fibroblasts with an anti-IL-4R mAb blocking ligand binding; 2) mast cell-derived IL-4 acts as a second signal for fibroblasts since it amplifies the action of low doses of obligatory fibroblast growth factors such as fibroblast growth factor or platelet-derived growth factor.
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44

Labanca, Estefania, Elba S. Vazquez, Paul G. Corn, Justin M. Roberts, Fen Wang, Christopher J. Logothetis, and Nora M. Navone. "Fibroblast growth factors signaling in bone metastasis." Endocrine-Related Cancer 27, no. 7 (July 2020): R255—R265. http://dx.doi.org/10.1530/erc-19-0472.

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Many solid tumors metastasize to bone, but only prostate cancer has bone as a single, dominant metastatic site. Recently, the FGF axis has been implicated in cancer progression in some tumors and mounting evidence indicate that it mediates prostate cancer bone metastases. The FGF axis has an important role in bone biology and mediates cell-to-cell communication. Therefore, we discuss here basic concepts of bone biology, FGF signaling axis, and FGF axis function in adult bone, to integrate these concepts in our current understanding of the role of FGF axis in bone metastases.
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45

Ray, L. B. "Enabling Endocrine Action of Fibroblast Growth Factors." Science's STKE 2007, no. 382 (April 10, 2007): tw133. http://dx.doi.org/10.1126/stke.3822007tw133.

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46

Terwisscha van Scheltinga, Afke F., Steven C. Bakker, René S. Kahn, and Martien J. H. Kas. "Fibroblast Growth Factors in Neurodevelopment and Psychopathology." Neuroscientist 19, no. 5 (January 23, 2013): 479–94. http://dx.doi.org/10.1177/1073858412472399.

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47

Krejci, P., P. B. Mekikian, and W. R. Wilcox. "The fibroblast growth factors in multiple myeloma." Leukemia 20, no. 6 (April 6, 2006): 1165–68. http://dx.doi.org/10.1038/sj.leu.2404202.

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48

Baird, A. "Fibroblast growth factors: what's in a name?" Endocrinology 132, no. 2 (February 1993): 487–88. http://dx.doi.org/10.1210/endo.132.2.8425469.

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49

Jeffers, Michael, William J. LaRochelle, and Henri S. Lichenstein. "Fibroblast growth factors in cancer: therapeutic possibilities." Expert Opinion on Therapeutic Targets 6, no. 4 (August 2002): 469–82. http://dx.doi.org/10.1517/14728222.6.4.469.

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Sensenbrenner, M. "The neurotrophic activity of fibroblast growth factors." Progress in Neurobiology 41, no. 6 (December 1993): 683–704. http://dx.doi.org/10.1016/0301-0082(93)90031-m.

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