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Journal articles on the topic 'TGF-beta'

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Published: 4 June 2021

Last updated: 9 June 2025

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1

Parekh, T., B. Saxena, J. Reibman, B. N. Cronstein, and L. I. Gold. "Neutrophil chemotaxis in response to TGF-beta isoforms (TGF-beta 1, TGF-beta 2, TGF-beta 3) is mediated by fibronectin." Journal of Immunology 152, no. 5 (March 1, 1994): 2456–66. http://dx.doi.org/10.4049/jimmunol.152.5.2456.

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Abstract TGF-beta isoforms regulate numerous cellular functions including cell growth and differentiation, the cellular synthesis and secretion of extracellular matrix proteins, such as fibronectin (Fn), and the immune response. We have previously shown that TGF-beta 1 is the most potent chemoattractant described for human peripheral blood neutrophils (PMNs), suggesting that TGF-beta s may play a role in the recruitment of PMNs during the initial phase of the inflammatory response. In our current studies, we demonstrate that the maximal chemotactic response was attained near 40 fM for all mamm

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2

Bascom, C. C., J. R. Wolfshohl, R. J. Coffey, L. Madisen, N. R. Webb, A. R. Purchio, R. Derynck, and H. L. Moses. "Complex regulation of transforming growth factor beta 1, beta 2, and beta 3 mRNA expression in mouse fibroblasts and keratinocytes by transforming growth factors beta 1 and beta 2." Molecular and Cellular Biology 9, no. 12 (December 1989): 5508–15. http://dx.doi.org/10.1128/mcb.9.12.5508-5515.1989.

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Regulation of transforming growth factor beta 1 (TGF beta 1), TGF beta 2, and TGF beta 3 mRNAs in murine fibroblasts and keratinocytes by TGF beta 1 and TGF beta 2 was studied. In quiescent AKR-2B fibroblasts, in which TGF beta induces delayed stimulation of DNA synthesis, TGF beta 1 autoregulation of TGF beta 1 expression was observed as early as 1 h, with maximal induction (25-fold) after 6 to 12 h. Increased expression of TGF beta 1 mRNA was accompanied by increased TGF beta protein production into conditioned medium of AKR-2B cells. Neither TGF beta 2 nor TGF beta 3 mRNA, however, was sign

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Bascom, C. C., J. R. Wolfshohl, R. J. Coffey, L. Madisen, N. R. Webb, A. R. Purchio, R. Derynck, and H. L. Moses. "Complex regulation of transforming growth factor beta 1, beta 2, and beta 3 mRNA expression in mouse fibroblasts and keratinocytes by transforming growth factors beta 1 and beta 2." Molecular and Cellular Biology 9, no. 12 (December 1989): 5508–15. http://dx.doi.org/10.1128/mcb.9.12.5508.

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Regulation of transforming growth factor beta 1 (TGF beta 1), TGF beta 2, and TGF beta 3 mRNAs in murine fibroblasts and keratinocytes by TGF beta 1 and TGF beta 2 was studied. In quiescent AKR-2B fibroblasts, in which TGF beta induces delayed stimulation of DNA synthesis, TGF beta 1 autoregulation of TGF beta 1 expression was observed as early as 1 h, with maximal induction (25-fold) after 6 to 12 h. Increased expression of TGF beta 1 mRNA was accompanied by increased TGF beta protein production into conditioned medium of AKR-2B cells. Neither TGF beta 2 nor TGF beta 3 mRNA, however, was sign

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4

ten Dijke, P., K. K. Iwata, C. Goddard, C. Pieler, E. Canalis, T. L. McCarthy, and M. Centrella. "Recombinant transforming growth factor type beta 3: biological activities and receptor-binding properties in isolated bone cells." Molecular and Cellular Biology 10, no. 9 (September 1990): 4473–79. http://dx.doi.org/10.1128/mcb.10.9.4473-4479.1990.

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We have recently cloned the cDNA for transforming growth factor type beta 3 (TGF-beta 3), a new member of the TGF-beta gene family. We examined the biological effects of recombinant TGF-beta 3 protein in osteoblast-enriched bone cell cultures. In this report we demonstrate that TGF-beta 3 is a potent regulator of functions associated with bone formation, i.e., mitogenesis, collagen synthesis, and alkaline phosphatase activity. In a direct comparison between TGF-beta 3 and TGF-beta 1, TGF-beta 3 appeared to be three- to fivefold more potent than TGF-beta 1. Our cross-linking experiments with io

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5

ten Dijke, P., K. K. Iwata, C. Goddard, C. Pieler, E. Canalis, T. L. McCarthy, and M. Centrella. "Recombinant transforming growth factor type beta 3: biological activities and receptor-binding properties in isolated bone cells." Molecular and Cellular Biology 10, no. 9 (September 1990): 4473–79. http://dx.doi.org/10.1128/mcb.10.9.4473.

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We have recently cloned the cDNA for transforming growth factor type beta 3 (TGF-beta 3), a new member of the TGF-beta gene family. We examined the biological effects of recombinant TGF-beta 3 protein in osteoblast-enriched bone cell cultures. In this report we demonstrate that TGF-beta 3 is a potent regulator of functions associated with bone formation, i.e., mitogenesis, collagen synthesis, and alkaline phosphatase activity. In a direct comparison between TGF-beta 3 and TGF-beta 1, TGF-beta 3 appeared to be three- to fivefold more potent than TGF-beta 1. Our cross-linking experiments with io

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6

Nunes, I., R. L. Shapiro, and D. B. Rifkin. "Characterization of latent TGF-beta activation by murine peritoneal macrophages." Journal of Immunology 155, no. 3 (August 1, 1995): 1450–59. http://dx.doi.org/10.4049/jimmunol.155.3.1450.

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Abstract Transforming growth factor-beta (TGF-beta) is secreted by most cells as a biologically inactive complex, called the large latent TGF-beta complex. The complex is comprised of latent TGF-beta binding protein (LTBP) and latent TGF-beta, which is mature TGF-beta associated noncovalently with its amino-terminal propeptides. LTBP is disulfide-linked to the amino-terminal propeptide of latent TGF-beta. Active TGF-beta is generated by release of TGF-beta from the complex. Generation of active TGF-beta by macrophages has been reported, but the activation mechanism has not been described. Late

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7

Villiger, P. M., A. B. Kusari, P. ten Dijke, and M. Lotz. "IL-1 beta and IL-6 selectively induce transforming growth factor-beta isoforms in human articular chondrocytes." Journal of Immunology 151, no. 6 (September 15, 1993): 3337–44. http://dx.doi.org/10.4049/jimmunol.151.6.3337.

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Abstract Transforming growth factor-beta (TGF-beta) plays an important role in homeostasis of connective tissues, but regulation of its expression in mesenchymal cells is not well characterized. This study examines the effects of the cytokines IL-1 beta and IL-6 on expression of TGF-beta isoforms in human articular chondrocytes. IL-6 caused a fivefold increase, in the secretion of TGF-beta bioactivity by primary chondrocytes, whereas IL-1 beta showed only marginal stimulatory effects. Analysis by Northern blotting showed that IL-6 induced TGF-beta 1 gene expression but had no detectable effect

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8

Siepl, C., U. V. Malipiero, and A. Fontana. "Transforming growth factor-beta (TGF-beta)-resistant helper T lymphocyte clones show a concomitant loss of all three types of TGF-beta receptors." Journal of Immunology 146, no. 9 (May 1, 1991): 3063–67. http://dx.doi.org/10.4049/jimmunol.146.9.3063.

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Abstract Three ovalbumin-specific T helper cell lines (OVA-7T cells) that differ in their susceptibility to the immunosuppressive effects of transforming growth factor-beta (TGF-beta) were cloned. The frequency of TGF-beta-resistant OVA-7T cell clones correlated with the decline of TGF-beta sensitivity in the original OVA-7T parental cell lines. In TGF-beta-resistant OVA-7T cell clones, TGF-beta inhibited neither the growth of the T cells nor their secretion of granulocyte macrophage CSF. TGF-beta suppressed the expression of c-myc mRNA in OVA-7T-responder but not in OVA-7T-nonresponder cells.

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9

Pelton, R. W., B. Saxena, M. Jones, H. L. Moses, and L. I. Gold. "Immunohistochemical localization of TGF beta 1, TGF beta 2, and TGF beta 3 in the mouse embryo: expression patterns suggest multiple roles during embryonic development." Journal of Cell Biology 115, no. 4 (November 15, 1991): 1091–105. http://dx.doi.org/10.1083/jcb.115.4.1091.

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Isoform-specific antibodies to TGF beta 1, TGF beta 2, and TGF beta 3 proteins were generated and have been used to examine the expression of these factors in the developing mouse embryo from 12.5-18.5 d post coitum (d.p.c.). These studies demonstrate the initial characterization of both TGF beta 2 and beta 3 in mammalian embryogenesis and are compared with TGF beta 1. Expression of one or all three TGF beta proteins was observed in many tissues, e.g., cartilage, bone, teeth, muscle, heart, blood vessels, lung, kidney, gut, liver, eye, ear, skin, and nervous tissue. Furthermore, all three TGF

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10

Waltenberger, J., A. Wanders, B. Fellström, K. Miyazono, C. H. Heldin, and K. Funa. "Induction of transforming growth factor-beta during cardiac allograft rejection." Journal of Immunology 151, no. 2 (July 15, 1993): 1147–57. http://dx.doi.org/10.4049/jimmunol.151.2.1147.

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Abstract The polypeptides of the transforming growth factor-beta (TGF-beta) family are potent endogenous immuno-regulators. Using a rat cardiac allograft transplant model, we investigated the expression of the precursor forms of TGF-beta 1, TGF-beta 2, and TGF-beta 3 and the latent TGF-beta binding protein (LTBP) by immunohistochemistry. The activity of TGF-beta in the extracts from transplanted as well as normal hearts was measured using a bioassay, and Northern blot analysis was performed on RNA extracts. The transplanted hearts were analyzed both during acute rejection up to 6 days and duri

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11

Constam, D. B., J. Philipp, U. V. Malipiero, P. ten Dijke, M. Schachner, and A. Fontana. "Differential expression of transforming growth factor-beta 1, -beta 2, and -beta 3 by glioblastoma cells, astrocytes, and microglia." Journal of Immunology 148, no. 5 (March 1, 1992): 1404–10. http://dx.doi.org/10.4049/jimmunol.148.5.1404.

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Abstract The type beta transforming growth factors (TGF) are potent regulators of the growth and functions of lymphocytes and macrophages. Recently the human glioblastoma cell line 308 was shown to produce TGF-beta 2. The relevance of this finding was evaluated further by comparing human glioblastoma cells with their nontransformed animal counterpart, astrocytes, with regard to the production of the three TGF-beta isoforms observed so far in mammals. In this report astrocytes are demonstrated to secrete also TGF-beta 2 and to express TGF-beta 1, -beta 2, and -beta 3 mRNA in vitro. In contrast,

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12

Kehrl, J. H., L. M. Wakefield, A. B. Roberts, S. Jakowlew, M. Alvarez-Mon, R. Derynck, M. B. Sporn, and A. S. Fauci. "Production of transforming growth factor beta by human T lymphocytes and its potential role in the regulation of T cell growth." Journal of Experimental Medicine 163, no. 5 (May 1, 1986): 1037–50. http://dx.doi.org/10.1084/jem.163.5.1037.

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This study examines the potential role of transforming growth factor beta (TGF-beta) in the regulation of human T lymphocyte proliferation, and proposes that TGF-beta is an important autoregulatory lymphokine that limits T lymphocyte clonal expansion, and that TGF-beta production by T lymphocytes is important in T cell interactions with other cell types. TGF-beta was shown to inhibit IL-2-dependent T cell proliferation. The addition of picograms amounts of TGF-beta to cultures of IL-2-stimulated human T lymphocytes suppressed DNA synthesis by 60-80%. A potential mechanism of this inhibition wa

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13

Lee, H. M., and S. Rich. "Differential activation of CD8+ T cells by transforming growth factor-beta 1." Journal of Immunology 151, no. 2 (July 15, 1993): 668–77. http://dx.doi.org/10.4049/jimmunol.151.2.668.

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Abstract Transforming growth factor-beta (TGF-beta) is a highly conserved multifunctional factor that broadly regulates cell growth and differentiation, and exhibits diverse regulatory roles in the immune system. In contrast to other studies describing TGF-beta as a potent inhibitor of lymphocyte growth, we have shown previously that TGF-beta 1 can also costimulate proliferation of murine splenic T cells activated by immobilized anti-CD3 antibody. In the present studies, we further investigate the subsets of T cells that are responsive to TGF-beta 1 costimulation. T cells were isolated into CD

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14

Sato, Y., R. Tsuboi, R. Lyons, H. Moses, and D. B. Rifkin. "Characterization of the activation of latent TGF-beta by co-cultures of endothelial cells and pericytes or smooth muscle cells: a self-regulating system." Journal of Cell Biology 111, no. 2 (August 1, 1990): 757–63. http://dx.doi.org/10.1083/jcb.111.2.757.

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The conversion of latent transforming growth factor beta (LTGF-beta) to the active species, transforming growth factor beta (TGF-beta), has been characterized in heterotypic cultures of bovine aortic endothelial (BAE) cells and bovine smooth muscle cells (SMCs). The formation of TGF-beta in co-cultures of BAE cells and SMCs was documented by a specific radioreceptor competition assay, while medium from homotypic cultures of BAE cells or SMCs contained no active TGF-beta as determined by this assay. The concentration of TGF-beta in the conditioned medium of heterotypic co-cultures was estimated

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15

Lafyatis, R., R. Lechleider, A. B. Roberts, and M. B. Sporn. "Secretion and transcriptional regulation of transforming growth factor-beta 3 during myogenesis." Molecular and Cellular Biology 11, no. 7 (July 1991): 3795–803. http://dx.doi.org/10.1128/mcb.11.7.3795-3803.1991.

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Transforming growth factor-beta 3 (TGF-beta 3) mRNA is differentially expressed in developing and mature mouse tissues, including high-level expression in developing and adult cardiac tissue. We show now that TGF-beta 3 mRNA is also expressed highly in skeletal muscle as well as in the mouse skeletal myoblast cell line C2C12. We also show that C2C12 cells secrete TGF-beta 3, and that this TGF-beta is able to inhibit C2C12 myoblast fusion after activation. In order to begin to understand how the TGF-beta 3 promoter is regulated in specific tissues during development, we therefore studied the re

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Lafyatis, R., R. Lechleider, A. B. Roberts, and M. B. Sporn. "Secretion and transcriptional regulation of transforming growth factor-beta 3 during myogenesis." Molecular and Cellular Biology 11, no. 7 (July 1991): 3795–803. http://dx.doi.org/10.1128/mcb.11.7.3795.

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Transforming growth factor-beta 3 (TGF-beta 3) mRNA is differentially expressed in developing and mature mouse tissues, including high-level expression in developing and adult cardiac tissue. We show now that TGF-beta 3 mRNA is also expressed highly in skeletal muscle as well as in the mouse skeletal myoblast cell line C2C12. We also show that C2C12 cells secrete TGF-beta 3, and that this TGF-beta is able to inhibit C2C12 myoblast fusion after activation. In order to begin to understand how the TGF-beta 3 promoter is regulated in specific tissues during development, we therefore studied the re

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17

Kehrl, J. H., A. S. Taylor, G. A. Delsing, A. B. Roberts, M. B. Sporn, and A. S. Fauci. "Further studies of the role of transforming growth factor-beta in human B cell function." Journal of Immunology 143, no. 6 (September 15, 1989): 1868–74. http://dx.doi.org/10.4049/jimmunol.143.6.1868.

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Abstract This study was designed to address three specific questions in human B cells. First, to determine whether transforming growth factor-beta (TGF-beta)2 has similar biologic effects on B cell function as does TGF-beta 1. Second, to test the hypothesis that TGF-beta 1 is an autocrine growth and differentiation inhibitor. Finally, because multiple receptor species for TGF-beta have been identified on other cell types, to determine by chemical cross-linking and competitive binding studies the nature of the TGF-beta 1 R present on normal and transformed B cells. Exogenous TGF-beta 2 was foun

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Thorp, B. H., I. Anderson, and S. B. Jakowlew. "Transforming growth factor-beta 1, -beta 2 and -beta 3 in cartilage and bone cells during endochondral ossification in the chick." Development 114, no. 4 (April 1, 1992): 907–11. http://dx.doi.org/10.1242/dev.114.4.907.

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The localization of TGF-beta 1, -beta 2 and -beta 3 was studied in the growth plate, epiphysis and metaphysis of the tibiotarsus of three-week-old chicks. The different TGF-beta isoforms were localized to hypertrophic chondrocytes, chondroclasts, osteoblasts and osteoclasts using immunohistochemical staining analysis with specific TGF-beta antibodies. TGF-betas in osteoclasts and chondroclasts were restricted to those cells located on the respective matrices. TGF-beta 3 localization was mainly cytoplasmic in the transitional (early hypertrophic) chondrocytes, but nuclear staining was also dete

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Jacobsen, SE, JR Keller, FW Ruscetti, P. Kondaiah, AB Roberts, and LA Falk. "Bidirectional effects of transforming growth factor beta (TGF-beta) on colony-stimulating factor-induced human myelopoiesis in vitro: differential effects of distinct TGF-beta isoforms." Blood 78, no. 9 (November 1, 1991): 2239–47. http://dx.doi.org/10.1182/blood.v78.9.2239.2239.

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Abstract Transforming growth factor-beta (TGF-beta) has potent antiproliferative effects on human hematopoietic progenitor cells. We report here that TGF-beta 1 and -beta 2 also exert bimodal dose-dependent stimulation of granulocyte-macrophage colony-stimulating factor (CSF) and granulocyte- CSF-induced day 7 granulocyte-macrophage colony-forming units. This increase in colony formation was restricted to low doses (0.01 to 1.0 ng/mL) of TGF-beta 1 and was due to increased granulopoiesis, showing that TGF-beta can affect the differentiation as well as the proliferation of hematopoietic progeni

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Jacobsen, SE, JR Keller, FW Ruscetti, P. Kondaiah, AB Roberts, and LA Falk. "Bidirectional effects of transforming growth factor beta (TGF-beta) on colony-stimulating factor-induced human myelopoiesis in vitro: differential effects of distinct TGF-beta isoforms." Blood 78, no. 9 (November 1, 1991): 2239–47. http://dx.doi.org/10.1182/blood.v78.9.2239.bloodjournal7892239.

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Transforming growth factor-beta (TGF-beta) has potent antiproliferative effects on human hematopoietic progenitor cells. We report here that TGF-beta 1 and -beta 2 also exert bimodal dose-dependent stimulation of granulocyte-macrophage colony-stimulating factor (CSF) and granulocyte- CSF-induced day 7 granulocyte-macrophage colony-forming units. This increase in colony formation was restricted to low doses (0.01 to 1.0 ng/mL) of TGF-beta 1 and was due to increased granulopoiesis, showing that TGF-beta can affect the differentiation as well as the proliferation of hematopoietic progenitors. Fur

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21

Mahmood, R., K. C. Flanders, and G. M. Morriss-Kay. "Interactions between retinoids and TGF beta s in mouse morphogenesis." Development 115, no. 1 (May 1, 1992): 67–74. http://dx.doi.org/10.1242/dev.115.1.67.

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Using immunocytochemical methods we describe the distribution of different TGF beta isoforms and the effects of excess retinoic acid on their expression during early mouse embryogenesis (8 1/2 - 10 1/2 days of development). In normal embryos at 9 days, intracellular TGF beta 1 is expressed most intensely in neuroepithelium and cardiac myocardium whereas extracellular TGF beta 1 is expressed in mesenchymal cells and in the endocardium of the heart. At later stages, intracellular TGF beta 1 becomes very restricted to the myocardium and to a limited number of head mesenchymal cells; extracellular

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22

Jacobsen, S. E., F. W. Ruscetti, A. B. Roberts, and J. R. Keller. "TGF-beta is a bidirectional modulator of cytokine receptor expression on murine bone marrow cells. Differential effects of TGF-beta 1 and TGF-beta 3." Journal of Immunology 151, no. 9 (November 1, 1993): 4534–44. http://dx.doi.org/10.4049/jimmunol.151.9.4534.

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Abstract Transforming growth factor beta (TGF-beta), an immunomodulator, has inhibitory as well as stimulatory effects on bone marrow cells. In this study, we demonstrate that TGF-beta 1 also is a bidirectional modulator of CSF receptor expression on murine bone marrow cells. TGF-beta 1 up-regulated granulocyte-macrophage (GM)-CSF receptor expression in a time- and dose-dependent manner, with a maximum up-regulation of 64% by 48 h at 20 ng/ml. In contrast, TGF-beta 1 down-modulated IL-3 and CSF-1 receptor expression by 54 and 55%, respectively, by 24 h. TGF-beta 1 did not affect G-CSF receptor

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23

Lamarre, J., J. Vasudevan та S. L. Gonias. "Plasmin cleaves betaglycan and releases a 60 kDa transforming growth factor-β complex from the cell surface". Biochemical Journal 302, № 1 (15 серпня 1994): 199–205. http://dx.doi.org/10.1042/bj3020199.

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Plasmin regulates the activity and distribution of transforming growth factor beta (TGF-beta) and other growth factors. The purpose of the present investigation was to determine the effects of plasmin on cellular receptors for TGF-beta. AKR-2B fibroblasts were affinity-labelled with 125I-TGF-beta 1 and 125I-TGF-beta 2, demonstrating betaglycan, the type-I TGF-beta receptor and the type-II TGF-beta receptor. Treatment of TGF-beta-affinity-labelled cells with plasmin (10-100 nM) for 1 h profoundly and selectively decreased recovery of TGF-beta-betaglycan complex. The type-I and type-II receptors

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24

Robinson, S. D., G. B. Silberstein, A. B. Roberts, K. C. Flanders, and C. W. Daniel. "Regulated expression and growth inhibitory effects of transforming growth factor-beta isoforms in mouse mammary gland development." Development 113, no. 3 (November 1, 1991): 867–78. http://dx.doi.org/10.1242/dev.113.3.867.

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Transforming Growth Factor-beta 1 (TGF-beta 1) was previously shown to inhibit reversibly the growth of mouse mammary ducts when administered in vivo by miniature slow-release plastic implants. We now report a comparative analysis of three TGF-beta isoforms with respect to gene expression and localization of protein products within the mouse mammary gland. Our studies revealed overlapping expression patterns of TGF-beta 1, TGF-beta 2 and TGF-beta 3 within the epithelium of the actively-growing mammary end buds during branching morphogenesis, as well as within the epithelium of growth-quiescent

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Tamaki, K., S. Okuda, M. Nakayama, T. Yanagida, and M. Fujishima. "Transforming growth factor-beta 1 in hypertensive renal injury in Dahl salt-sensitive rats." Journal of the American Society of Nephrology 7, no. 12 (December 1996): 2578–89. http://dx.doi.org/10.1681/asn.v7122578.

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The expression of transforming growth factor-beta 1 (TGF-beta 1) for hypertensive renal injury was investigated in Dahl salt-sensitive (Dahl-S) rats fed a high-salt (HS; 8% NaCl) diet or a low-salt (LS; 0.3% NaCl) diet for 4 wk. The HS rats developed severe hypertension and renal damage, including glomerulosclerosis and arteriosclerosis. TGF-beta biosynthesis by isolated glomeruli, the TGF-beta localization, and the gene expression of TGF-beta 1, latent TGF-beta binding protein (LTBP), and TGF-beta receptors (Types I, II, and III) were compared between the HS rats and LS rats. A TGF-beta bioas

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Mitchell, E. J., K. Lee, and M. D. O'Connor-McCourt. "Characterization of transforming growth factor-beta (TGF-beta) receptors on BeWo choriocarcinoma cells including the identification of a novel 38-kDa TGF-beta binding glycoprotein." Molecular Biology of the Cell 3, no. 11 (November 1992): 1295–307. http://dx.doi.org/10.1091/mbc.3.11.1295.

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Transforming growth factor-beta (TGF-beta) is a potential mediator of placental trophoblast functions, including differentiation, hormone production, endometrial invasion, and immunosuppression. Equilibrium binding and affinity-labeling assays were used to investigate the binding characteristics of TGF-beta 1 and TGF-beta 2 on an established human choriocarcinoma trophoblastic cell line (BeWo). The equilibrium binding experiments indicated that the BeWo cells exhibited similar average affinities and total number of binding sites for TGF-beta 1 and TGF-beta 2. The Kd values obtained from Scatch

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27

Bodmer, S., K. Strommer, K. Frei, C. Siepl, N. de Tribolet, I. Heid, and A. Fontana. "Immunosuppression and transforming growth factor-beta in glioblastoma. Preferential production of transforming growth factor-beta 2." Journal of Immunology 143, no. 10 (November 15, 1989): 3222–29. http://dx.doi.org/10.4049/jimmunol.143.10.3222.

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Abstract Transforming growth factor (TGF)-beta 1 is a polypeptide that is assumed to play a fundamental role in the growth of both normal and neoplastic cells. TGF-beta 2 is a closely related polypeptide, originally described as glioblastoma cell-derived T cell suppressor factor (G-TsF) due to its immunosuppressive activity. Expression of the genes for TGF-beta 1 and G-TsF/TGF-beta 2 was examined in tumor cells and was found to be different in several cell lines and tissues that were tested. Whereas two glioblastoma cell lines expressed both TGF-beta 1 and G-TsF/TGF-beta 2 mRNA, one melanoma a

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28

Guh, J. Y., M. L. Yang, Y. L. Yang, C. C. Chang, and L. Y. Chuang. "Captopril reverses high-glucose-induced growth effects on LLC-PK1 cells partly by decreasing transforming growth factor-beta receptor protein expressions." Journal of the American Society of Nephrology 7, no. 8 (August 1996): 1207–15. http://dx.doi.org/10.1681/asn.v781207.

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Transforming growth factor beta (TGF-beta) may be important in the pathogenesis of diabetic nephropathy, and captopril is effective in treating this disorder. However, the mechanisms of this therapeutic effect as related to TGF-beta and its receptors are not known. Thus, the effects of captopril on cellular growth, TGF-beta 1, and TGF-beta receptors were studied in LLC-PK1 cells cultured in normal (11 mM) or high glucose (27.5 mM). This study found that glucose dose-dependently inhibited cellular mitogenesis while inducing hypertrophy in these cells at 72 h of culture, concomitantly with enhan

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29

Saksela, O., D. Moscatelli, and D. B. Rifkin. "The opposing effects of basic fibroblast growth factor and transforming growth factor beta on the regulation of plasminogen activator activity in capillary endothelial cells." Journal of Cell Biology 105, no. 2 (August 1, 1987): 957–63. http://dx.doi.org/10.1083/jcb.105.2.957.

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Basic fibroblast growth factor (bFGF), a potent inducer of angiogenesis in vivo, stimulates the production of both urokinase- and tissue-type plasminogen activators (PAs) in cultured bovine capillary endothelial cells. The observed increase in proteolytic activity induced by bFGF was effectively diminished by picogram amounts of transforming growth factor beta (TGF beta), but could not be abolished by increasing the amount of TGF beta. However, the inhibition by TGF beta was greatly enhanced if the cells were pretreated with TGF beta before addition of bFGF. After prolonged incubation of cultu

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Olson, E. N., E. Sternberg, J. S. Hu, G. Spizz, and C. Wilcox. "Regulation of myogenic differentiation by type beta transforming growth factor." Journal of Cell Biology 103, no. 5 (November 1, 1986): 1799–805. http://dx.doi.org/10.1083/jcb.103.5.1799.

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Type beta transforming growth factor (TGF beta) has been shown to be both a positive and negative regulator of cellular proliferation and differentiation. The effects of TGF beta also are cell-type specific and appear to be modulated by other growth factors. In the present study, we examined the potential of TGF beta for control of myogenic differentiation. In mouse C-2 myoblasts, TGF beta inhibited fusion and prevented expression of the muscle-specific gene products, creatine kinase and acetylcholine receptor. Differentiation of the nonfusing muscle cell line, BC2Hl, was also inhibited by TGF

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McCaffrey, T. A., D. J. Falcone, C. F. Brayton, L. A. Agarwal, F. G. Welt, and B. B. Weksler. "Transforming growth factor-beta activity is potentiated by heparin via dissociation of the transforming growth factor-beta/alpha 2-macroglobulin inactive complex." Journal of Cell Biology 109, no. 1 (July 1, 1989): 441–48. http://dx.doi.org/10.1083/jcb.109.1.441.

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The control of smooth muscle cell (SMC) proliferation is determined by the combined actions of mitogens, such as platelet-derived growth factor, and the opposing action of growth inhibitory agents, such as heparin and transforming growth factor-beta (TGF-beta). The present studies identify an interaction between heparin and TGF-beta in which heparin potentiates the biological action of TGF-beta. Using a neutralizing antibody to TGF-beta, we observed that the short term antiproliferative effect of heparin depended upon the presence of biologically active TGF-beta. This effect was observed in ra

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Kim, S. J., J. H. Kehrl, J. Burton, C. L. Tendler, K. T. Jeang, D. Danielpour, C. Thevenin, K. Y. Kim, M. B. Sporn, and A. B. Roberts. "Transactivation of the transforming growth factor beta 1 (TGF-beta 1) gene by human T lymphotropic virus type 1 tax: a potential mechanism for the increased production of TGF-beta 1 in adult T cell leukemia." Journal of Experimental Medicine 172, no. 1 (July 1, 1990): 121–29. http://dx.doi.org/10.1084/jem.172.1.121.

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We examined the effect of the human T lymphotropic virus type 1 (HTLV-I) Tax gene product on the human transforming growth factor beta 1 (TGF-beta 1) promoter. Transfection of deleted constructs of the TGF-beta 1 promoter revealed regions homologous with AP-1 binding sites that were required for Tax-induced transactivation of the TGF-beta 1 promoter. In addition, we examined the expression and secretion of TGF-beta in fresh leukemic cells isolated from patients with adult T cell leukemia (ATL) and in HTLV-1-infected T cell lines. We report that fresh leukemic cells from ATL patients constituti

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Rich, S., N. Van Nood, and H. M. Lee. "Role of alpha 5 beta 1 integrin in TGF-beta 1-costimulated CD8+ T cell growth and apoptosis." Journal of Immunology 157, no. 7 (October 1, 1996): 2916–23. http://dx.doi.org/10.4049/jimmunol.157.7.2916.

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Abstract TGF-beta 1 regulates cell growth, differentiation, and adhesion and is a potent immunosuppressant, in part through its well-recognized growth-inhibitory effects. However, certain T cell subsets, particularly of naive phenotype, can instead be costimulated to proliferate by TGF-beta 1. We have previously demonstrated that naive murine CD8+ T cells, TCR activated by platebound anti-CD3 Ab or SEB superantigen, are growth stimulated by TGF-beta 1, acquire a memory phenotype, express elevated IL-10 and TGF-beta 1, and cause T cell growth inhibition as effector CD8+ T cells. TGF-beta 1 caus

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Arrick, B. A., A. R. Lopez, F. Elfman, R. Ebner, C. H. Damsky, and R. Derynck. "Altered metabolic and adhesive properties and increased tumorigenesis associated with increased expression of transforming growth factor beta 1." Journal of Cell Biology 118, no. 3 (August 1, 1992): 715–26. http://dx.doi.org/10.1083/jcb.118.3.715.

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Transforming growth factor-beta (TGF-beta) is a potent mediator of cell proliferation and extracellular matrix formation, depending on the cell type and the physiological conditions. TGF-beta is usually secreted in a "latent" complex that needs activation before it can exert its effects. Several observations correlate increased expression of TGF-beta 1 with tumorigenesis. To evaluate the physiological relevance of increased TGF-beta 1 synthesis in tumor cells we established cell clones overexpressing TGF-beta 1 and observed the resulting physiological changes in TGF-beta overproducing cells in

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Elias, J. A., V. Lentz, and P. J. Cummings. "Transforming growth factor-beta regulation of IL-6 production by unstimulated and IL-1-stimulated human fibroblasts." Journal of Immunology 146, no. 10 (May 15, 1991): 3437–43. http://dx.doi.org/10.4049/jimmunol.146.10.3437.

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Abstract We characterized the ability of transforming growth factor-beta 1 (TGF-beta 1) and transforming growth factor-beta 2 (TGF-beta 2) to regulate IL-6 production by unstimulated and rIL-1-stimulated lung fibroblasts. rTGF-beta 1-, purified TGF-beta 1-, and purified TGF-beta 2-stimulated fibroblasts produced IL-6 bioactivity as assessed with the B9 hybridoma proliferation assay. These TGF-beta moieties also bidirectionally regulated the IL-6 production of rIL-1-stimulated fibroblasts. The addition of TGF-beta to cultures in which fibroblasts were vigorously stimulated with rIL-1 resulted i

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Lopez, A. R., J. Cook, P. L. Deininger, and R. Derynck. "Dominant negative mutants of transforming growth factor-beta 1 inhibit the secretion of different transforming growth factor-beta isoforms." Molecular and Cellular Biology 12, no. 4 (April 1992): 1674–79. http://dx.doi.org/10.1128/mcb.12.4.1674-1679.1992.

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Transforming growth factor-beta (TGF-beta) is a secreted polypeptide factor that is thought to play a major role in the regulation of proliferation of many cell types and various differentiation processes. Several related isoforms have been structurally characterized, three of which, TGF-beta 1, -beta 2, and -beta 3, have been detected in mammalian cells and tissues. Each TGF-beta form is a homodimer of a 112-amino-acid polypeptide which is encoded as a larger polypeptide precursor. We have introduced several mutations in the TGF-beta 1 precursor domain, resulting in an inhibition of TGF-beta

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Lopez, A. R., J. Cook, P. L. Deininger, and R. Derynck. "Dominant negative mutants of transforming growth factor-beta 1 inhibit the secretion of different transforming growth factor-beta isoforms." Molecular and Cellular Biology 12, no. 4 (April 1992): 1674–79. http://dx.doi.org/10.1128/mcb.12.4.1674.

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Transforming growth factor-beta (TGF-beta) is a secreted polypeptide factor that is thought to play a major role in the regulation of proliferation of many cell types and various differentiation processes. Several related isoforms have been structurally characterized, three of which, TGF-beta 1, -beta 2, and -beta 3, have been detected in mammalian cells and tissues. Each TGF-beta form is a homodimer of a 112-amino-acid polypeptide which is encoded as a larger polypeptide precursor. We have introduced several mutations in the TGF-beta 1 precursor domain, resulting in an inhibition of TGF-beta

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Kehrl, J. H., A. B. Roberts, L. M. Wakefield, S. Jakowlew, M. B. Sporn, and A. S. Fauci. "Transforming growth factor beta is an important immunomodulatory protein for human B lymphocytes." Journal of Immunology 137, no. 12 (December 15, 1986): 3855–60. http://dx.doi.org/10.4049/jimmunol.137.12.3855.

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Abstract The growth and differentiation of B cells to immunoglobulin (Ig)-secreting cells is regulated by a variety of soluble factors. This study presents data that support a role for transforming growth factor (TGF)-beta in this regulatory process. B lymphocytes were shown to have high-affinity receptors for TGF-beta that were increased fivefold to sixfold after in vitro activation. The addition of picogram quantities of TGF-beta to B cell cultures suppressed factor-dependent, interleukin 2 (IL 2) B cell proliferation and markedly suppressed factor-dependent (IL 2 or B cell differentiation f

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Altman, D. J., S. L. Schneider, D. A. Thompson, H. L. Cheng, and T. B. Tomasi. "A transforming growth factor beta 2 (TGF-beta 2)-like immunosuppressive factor in amniotic fluid and localization of TGF-beta 2 mRNA in the pregnant uterus." Journal of Experimental Medicine 172, no. 5 (November 1, 1990): 1391–401. http://dx.doi.org/10.1084/jem.172.5.1391.

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This report describes a murine amniotic fluid (MAF) immunosuppressive factor that has properties similar to transforming growth factor beta (TGF-beta). The MAF factor exhibits TGF-beta-like activity in stimulating soft agar colony formation by AKR-2B cells and inhibiting thymidine uptake by Mv1Lu cells. We demonstrate that both the immunosuppressive and TGF-beta-like activities of the MAF factor are completely neutralized by anti-TGF-beta 2-specific antibodies and not by anti-TGF-beta 1-specific antisera. The immunosuppressive factor in MAF is novel in that it appears to be identical or very c

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Akhurst, R. J., S. A. Lehnert, A. Faissner, and E. Duffie. "TGF beta in murine morphogenetic processes: the early embryo and cardiogenesis." Development 108, no. 4 (April 1, 1990): 645–56. http://dx.doi.org/10.1242/dev.108.4.645.

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The tissue distribution of TGF beta-1 RNA was examined within whole mouse embryos from implantation to 10.5 days gestational age and, in the developing heart, up to 8 days postpartum. The earliest high level expression of TGF beta-1 RNA is at 7.0 days postcoitum (p.c.) in the cardiac mesoderm. At 8.0 days gestational age, cardiac TGF beta-1 RNA expression is limited to endocardial cells. By 9.5 days p.c., this expression pattern becomes regionalized to those cells that overlie cardiac cushion tissue. High TGF beta-1 RNA levels continue to persist in endothelial cells of the heart valves until

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Murphy-Ullrich, J. E., S. Schultz-Cherry, and M. Höök. "Transforming growth factor-beta complexes with thrombospondin." Molecular Biology of the Cell 3, no. 2 (February 1992): 181–88. http://dx.doi.org/10.1091/mbc.3.2.181.

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Thrombospondin (TSP) was demonstrated to inhibit the growth of bovine aortic endothelial cells, an activity that was not neutralized by antibodies to TSP or by other agents that block TSP-cell interactions but that partially was reversed by a neutralizing antibody to transforming growth factor-beta (TGF-beta). Similar to TGF-beta, TSP supported the growth of NRK-49F colonies in soft agar in a dose-dependent manner, which required epidermal growth factor and was neutralized by anti-TGF-beta antibody. Chromatography of a TSP preparation did not separate the TGF-beta-like NRK colony-forming activ

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Samuel, S. K., R. A. Hurta, M. A. Spearman, J. A. Wright, E. A. Turley, and A. H. Greenberg. "TGF-beta 1 stimulation of cell locomotion utilizes the hyaluronan receptor RHAMM and hyaluronan." Journal of Cell Biology 123, no. 3 (November 1, 1993): 749–58. http://dx.doi.org/10.1083/jcb.123.3.749.

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TGF-beta is a potent stimulator of motility in a variety of cell types. It has recently been shown that hyaluronan (HA) can directly promote locomotion of cells through interaction with the HA receptor RHAMM. We have investigated the role of RHAMM and HA in TGF-beta-stimulated locomotion and show that TGF-beta triggers the transcription, synthesis and membrane expression of the RHAMM receptor and the secretion of HA coincident with the induction of the locomotory response. This was demonstrated by both incubating cells with exogenous TGF-beta 1 and by stimulating the production of bioactive TG

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Clark, D. A., K. C. Flanders, D. Banwatt, W. Millar-Book, J. Manuel, J. Stedronska-Clark, and B. Rowley. "Murine pregnancy decidua produces a unique immunosuppressive molecule related to transforming growth factor beta-2." Journal of Immunology 144, no. 8 (April 15, 1990): 3008–14. http://dx.doi.org/10.4049/jimmunol.144.8.3008.

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Abstract Non-T small lymphocytic suppressor cells in murine allopregnancy release a potent immunosuppressive factor in vitro that is neutralized by rabbit anti-transforming growth factor (TGF)-beta. Previous studies have suggested that the decidual suppressor factor (DSF) is smaller than TGF-beta 1, and in this paper, we show that DSF on HPLC-sieving columns also elutes later than TGF-beta 2. Nevertheless, DSF has the ability to promote anchorage-independent growth of NRK fibroblasts similar to TGF-beta s. Using turkey antibodies specific for TGF-beta 1 or beta 2, we show that DSF is related t

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Ridley, A. J., J. B. Davis, P. Stroobant, and H. Land. "Transforming growth factors-beta 1 and beta 2 are mitogens for rat Schwann cells." Journal of Cell Biology 109, no. 6 (December 1, 1989): 3419–24. http://dx.doi.org/10.1083/jcb.109.6.3419.

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Transforming growth factor-beta 1 (TGF-beta 1) and TGF-beta 2 were found to be potent mitogens for purified rat Schwann cells, each stimulating DNA synthesis in quiescent cells and also increasing their proliferation rate. Half-maximal stimulation of DNA synthesis occurred at approximately 0.1 ng/ml TGF-beta 1 or TGF-beta 2. Mitogenic stimulation by TGF-beta 1 and TGF-beta 2 was enhanced by forskolin, which activates adenylate cyclase, at concentrations up to 0.5 microM forskolin. However, at 5 microM forskolin, the synergistic interaction between forskolin and TGF-beta 1 was abolished. These

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Pelton, R. W., M. E. Dickinson, H. L. Moses, and B. L. Hogan. "In situ hybridization analysis of TGF beta 3 RNA expression during mouse development: comparative studies with TGF beta 1 and beta 2." Development 110, no. 2 (October 1, 1990): 609–20. http://dx.doi.org/10.1242/dev.110.2.609.

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To date, three closely-related TGF beta genes have been found in the mouse; TGF beta 1, TGF beta 2 and TGF beta 3. Previous experiments have indicated that TGF beta 1 and TGF beta 2 may play important roles during mouse embryogenesis. The present study now reports the distribution of transcripts of TGF beta 3 in comparison to the other two genes and reveals overlapping but distinct patterns of RNA expression. TGF beta 3 RNA is expressed in a diverse array of tissues including perichondrium, bone, intervertebral discs, mesenteries, pleura, heart, lung, palate, and amnion, as well as in central

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Wahl, S. M., D. A. Hunt, H. L. Wong, S. Dougherty, N. McCartney-Francis, L. M. Wahl, L. Ellingsworth, J. A. Schmidt, G. Hall, and A. B. Roberts. "Transforming growth factor-beta is a potent immunosuppressive agent that inhibits IL-1-dependent lymphocyte proliferation." Journal of Immunology 140, no. 9 (May 1, 1988): 3026–32. http://dx.doi.org/10.4049/jimmunol.140.9.3026.

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Abstract Transforming growth factor-beta (TGF-beta), a product of neoplastic and hemopoietic cells, is a bifunctional regulator of the immune response. At femtomolar concentrations, TGF-beta stimulates monocyte migration, and picomolar quantities induce synthesis of monocyte growth factors, including IL-1, that may promote tissue repair by regulating fibrosis and angiogenesis. Paradoxically, TGF-beta at picomolar concentrations also blocks the ability of IL-1 to stimulate lymphocyte proliferation. At 0.01 to 1.0 ng/ml, TGF-beta 1 and its homologue, TGF-beta 2, suppress the IL-1-dependent murin

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Lyons, R. M., L. E. Gentry, A. F. Purchio, and H. L. Moses. "Mechanism of activation of latent recombinant transforming growth factor beta 1 by plasmin." Journal of Cell Biology 110, no. 4 (April 1, 1990): 1361–67. http://dx.doi.org/10.1083/jcb.110.4.1361.

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Medium conditioned by Chinese hamster ovary (CHO) cells transfected with the simian pre-pro-TGF beta 1 cDNA contains high levels of latent TGF beta 1. The amino-terminal region of the TGF beta 1 precursor is secreted and can be detected in the conditioned medium by immunoblotting using peptide antibodies specific for amino-terminal peptides. Chemical cross-linking of CHO-conditioned medium using bis-(sulfosuccinimidyl)-suberate (BS3) followed by immunoblot analyses indicates that latent recombinant TGF beta 1 contains both the cleaved amino-terminal glycopeptide and mature TGF beta 1 polypepti

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Pehlivan, T., A. Mansour, RZ Spaczynski, and AJ Duleba. "Effects of transforming growth factors-alpha and -beta on proliferation and apoptosis of rat theca-interstitial cells." Journal of Endocrinology 170, no. 3 (September 1, 2001): 639–45. http://dx.doi.org/10.1677/joe.0.1700639.

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Ovarian development, follicular growth and atresia require mechanisms regulating proliferation and death of ovarian cells including theca-interstitial (T-I) cells. Transforming growth factors-alpha and -beta (TGF-alpha and TGF-beta) are well recognized local modulators of T-I function. This study was performed to evaluate the effects of TGF-alpha and TGF-beta on ovarian T-I cell proliferation, differentiation and apoptosis. T-I cells from immature Sprague-Dawley rats were purified and incubated in chemically defined media. Proliferation was assessed by [3H]thymidine incorporation assay and by

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Nogami, M., D. J. Romberger, S. I. Rennard, and M. L. Toews. "TGF-beta 1 modulates beta-adrenergic receptor number and function in cultured human tracheal smooth muscle cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 266, no. 2 (February 1, 1994): L187—L191. http://dx.doi.org/10.1152/ajplung.1994.266.2.l187.

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Pretreatment of cultured human tracheal smooth muscle cells with transforming growth factor-beta 1 (TGF-beta 1) decreased adenosine 3',5'-cyclic monophosphate (cAMP) accumulation by intact cells stimulated with the beta-adrenergic agonist isoproterenol. The maximal inhibition of isoproterenol-stimulated cAMP accumulation by TGF-beta 1 was 31 +/- 3%, and the mean effective concentration (EC50) of TGF-beta 1 was approximately 1.5 pM. TGF-beta 1 decreased the maximal response to isoproterenol but did not change the EC50 value of isoproterenol. TGF-beta 1 did not change cAMP accumulation stimulate

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Streuli, C. H., C. Schmidhauser, M. Kobrin, M. J. Bissell, and R. Derynck. "Extracellular matrix regulates expression of the TGF-beta 1 gene." Journal of Cell Biology 120, no. 1 (January 1, 1993): 253–60. http://dx.doi.org/10.1083/jcb.120.1.253.

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Transforming growth factor-beta (TGF-beta) is a potent regulator of cell proliferation and modulates the interactions of cells with their extracellular matrix (ECM), in part by inducing the synthesis of various ECM proteins. Three different isoforms of TGF-beta are synthesized in a defined pattern in specific cell populations in vivo. In the specific case of TGF-beta 1, this well-defined and limited expression stands in sharp contrast to its synthesis by virtually all cells in culture. Using mammary epithelial cells as a model system, we evaluated the substratum dependence of the expression of

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