Transforming growth factor type beta induces monocyte chemotaxis and growth factor production.

Wahl, Sharon M.; Hunt, D A; Wakefield, Lalage M.; McCartney-Francis, Nancy; Wahl, Larry M.; Roberts, Anita B.; Sporn, Michael B.

doi:10.1073/pnas.84.16.5788

Cited by 1,126 publications

(661 citation statements)

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“…To quantify the amplified transcripts, PCR was conducted by incorporation at 14-34 cycles using cDNA samples from FLS. The amounts of amplified products of MCAF and &m were exponential at [14][15][16][17][18][19][20][21][22][23][24][25][26] cycles and then decreased slowly (data not shown); PCR amplification of cDNA for MCAF and &m was consequently carried out for 20 cycles in this study. As shown in Figure 5 , 188 bp of MCAF transcripts were detected in FLS incubated with the medium alone.…”

Section: Resultsmentioning

confidence: 99%

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Expression of monocyte chemotactic and activating factor in rheumatoid arthritis. regulation of its production in synovial cells by interleukin‐1 and tumor necrosis factor

Akahoshi

Wada

Endo

et al. 1993

Arthritis & Rheumatism

110

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Objective. To investigate whether monocyte chemotactic and activating factor (MCAF) contributes to the accumulation of macrophages in the joints of patients with rheumatoid arthritis (RA). Methods. MCAF was measured by radioimmunoassay. MCAF gene expression was determined by Northern blotting and reverse‐transcriptase polymerase chain reaction. Recombinant human MCAF was injected into rabbit joints to evaluate the effect of MCAF on infiltration of macrophages. Results. High levels of MCAF were detected in synovial fluid from patients with RA. Cells freshly isolated from synovial fluid expressed MCAF messenger RNA (mRNA). Fibroblast‐like synoviocytes were found to express MCAF mRNA and to secrete MCAF in response to interleukin‐1 (IL‐1) and tumor necrosis factor in vitro. IL‐1 also promoted MCAF gene expression in rabbit synovial tissue in vivo. MCAF caused marked infiltration of macrophages in rabbit synovial tissue. Conclusion. Our findings suggest that MCAF may contribute to the accumulation of macrophages in inflamed rheumatoid joints.

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Section: Resultsmentioning

confidence: 99%

“…Transforming growth factor p (18,19) and granulocyte-macrophage colony-stimulating factor (GM-CSF) (20), both present in SF and synovial tissue of patients with RA, are active chemotactic factors for monocytes. The components of complement are also monocyte chemoattractants.…”

Section: Discussionmentioning

confidence: 99%

Expression of monocyte chemotactic and activating factor in rheumatoid arthritis. regulation of its production in synovial cells by interleukin‐1 and tumor necrosis factor

Akahoshi

Wada

Endo

et al. 1993

Arthritis & Rheumatism

110

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“…We have recently shown that TGF-,B1 administered over a protracted period of time can significantly suppress the proliferative activity in the small intestinal crypts, the effect being particularly pronounced in the stem cell region . In addition, TGF-ps can have the opposite effect on some cell types and act as indirect mitogens, particularly for mesenchymal cell types, and exert effects on chemotaxis and on the synthesis and degradation of extracellular matrix proteins (Ignotz and Massague 1986;Posthlethwaite et al, 1987;Wahl et al, 1987;Roberts and Sporn, 1991).…”

Section: Discussionmentioning

confidence: 99%

Pretreatment with transforming growth factor beta-3 protects small intestinal stem cells against radiation damage in vivo

Potten

Booth²,

Haley³

1997

Br J Cancer

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Summary The gastrointestinal tract, with its rapid cell replacement, is sensitive to cytotoxic damage and can be a site of dose-limiting toxicity in cancer therapy. Here, we have investigated the use of one growth modulator to manipulate the cell cycle status of gastrointestinal stem cells before cytotoxic exposure to minimize damage to this normal tissue. Transforming growth factor beta-3 (TGF-,3), a known inhibitor of cell cycle progression through G,, was used to alter intestinal crypt stem cell sensitivity before 12-16 Gy of gamma irradiation, which was used as a model cytotoxic agent. Using a crypt microcolony assay as a measure of functional competence of gastrointestinal stem cells, it was shown that the administration of TGF-P3 over a 24-h period before irradiation increased the number of surviving crypts by four-to six-fold.To test whether changes in crypt survival are reflected in the well-being of the animal, survival time analyses were performed. After 14.5 Gy of radiation, only 35% of the animals survived within a period of about 12 days, while prior treatment with TGF-,B3 provided significant protection against this early gastrointestinal animal death, with 95% of the treated animals surviving for greater than 30 days.

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“…It can be hypothesized that this could be due to a direct activity of the transgenic TGF␤1 on these cells. It has been observed before that this factor can be chemoattractant on human peripheral blood monocytes 21 and that it is also able to induce migratory gut-seeking lymphocytes to become resident within the intraepithelial compartment of the gut. 22,23 It is also possible that the accumulation of apoptotic cells that would result from the activity of the transgene on secretory hyperplastic lesions could attract mononuclear cells to the area.…”

Section: Weak Wap-tgf␤1 Tumor Inhibitory Effect May Be a Consequence mentioning

confidence: 96%

Impairment of mammary lobular development induced by expression of TGF?1 under the control of WAP promoter does not suppress tumorigenesis in MMTV-infected transgenic mice

et al. 2001

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It has previously been shown that transgenic female mice expressing TGF␤1 under control of regulatory elements of the whey-acidic protein (WAP) gene were unable to lactate. This was due to the increased apoptosis of the cells committed to the lobular-lactogenic phenotype. Our goal was to determine whether the expression of WAP-TGF␤1 transgene could inhibit MMTV (mouse mammary tumor virus) tumorigenic activity in the mammary gland. It is well known that the infection with this virus produces focal hyperplastic secretory nodules (HANs) and, some variants can also induce ductal pregnancy-dependent lesions (plaques). In either case, MMTV infection leads ultimately to the appearance of malignant mammary tumors. The results shown herein demonstrate that TGF␤1 expression in the secretory mammary epithelium does not suppress mammary tumorigenesis in MMTV infected mice. Although MMTV infected WAP-TGF␤1 transgenic females displayed a strong impairment of lobule-alveolar development, carcinogenesis induced by any of the four MMTV variants used herein proceeded unabated. WAP-TGF␤1 tumors that showed a strong expression at the WAP promoter, appeared later and grew more slowly than their wild-type counterparts. Transgenic females also had a lower incidence of HANs and plaques. Our study suggests that the epithelial target cells for tumorigenic mutations are probably progenitor cells that are not susceptible to the apoptotic effect of TGF␤1. Alternatively, their daughters cells that display the secretory phenotype and could be more involved in the formation of premalignant lesions continue to die due to the expression of the transgene. © 2001 Wiley-Liss, Inc. Key words: mammary tumor; MMTV; TGF␤1; stem cellsTransforming growth factor-␤1 is a member of a large superfamily of polypeptides and seems to affect many key events in normal growth and differentiation. 1,2 There is good evidence that members of the TGF␤1 gene family may indeed contribute essential signals for the development and secretory maturation of the mammary epithelium. An approach to TGF␤ function and mammary gland development has been the use of transgenic mice. TGF␤1 has been targeted to the mammary epithelium from different transcriptional promoters in two transgenic mouse models. In one, the mouse mammary tumor virus-long terminal repeat (MMTV-LTR) was used to promote expression of TGF␤1 in mammary epithelium. 3 In this biological model, a transient but distinct inhibition of mammary ductal extension and side branching was observed between 3 and 6 weeks of age; however subsequent development during pregnancy and lactation proceeded apparently unperturbed. In the second transgenic mouse model, TGF␤1 was expressed under the control of the whey acidic protein (WAP) promoter. This promoter is mammary epithelium-specific and most active during late pregnancy and lactation. In this model no inhibition of mammary ductal growth at puberty was observed. 4 With the onset of pregnancy, lobule-alveolar growth and development were impaired to the extent that lactation was...

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Transforming growth factor type beta induces monocyte chemotaxis and growth factor production.

Abstract: ABSTRACT

Cited by 1,126 publications

References 31 publications

Expression of monocyte chemotactic and activating factor in rheumatoid arthritis. regulation of its production in synovial cells by interleukin‐1 and tumor necrosis factor

Expression of monocyte chemotactic and activating factor in rheumatoid arthritis. regulation of its production in synovial cells by interleukin‐1 and tumor necrosis factor

Pretreatment with transforming growth factor beta-3 protects small intestinal stem cells against radiation damage in vivo

Impairment of mammary lobular development induced by expression of TGF?1 under the control of WAP promoter does not suppress tumorigenesis in MMTV-infected transgenic mice

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