Intragraft expression of transforming growth factor β1 gene in isolated glomeruli from human renal transplants

Nicholson, M. L.; Bicknell, G R; Barker, Gordon T.; Doughman, T; Williams, S.; Furness, Peter

doi:10.1046/j.1365-2168.1999.01202.x

Cited by 15 publications

(8 citation statements)

References 21 publications

(27 reference statements)

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“…Immunohistochemistry has shown that kidneys with CNI-induced morphologic abnormalities express the cytokine TGF-␤1 (21)(22)(23)(24). Furthermore, stimulation of the TGF-␤1 production in vivo after the use of CNI has been described by several groups.…”

Section: Discussionmentioning

confidence: 97%

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The Impact of Transforming Growth Factor-β1 Gene Polymorphism on End-Stage Renal Failure After Heart Transplantation

et al. 2006

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Section: Discussionmentioning

confidence: 97%

“…For codon 10, 82.5% in the ESRFϩ group versus 56.1% in the ESRF-group were Pro-carriers (Pϭ0.0003). For codon 25,24.6% in the ESRFϩ group versus 10% in the ESRF-group were Pro-carriers (Pϭ0.008). None of the patients who were homozygote for leucine at codon 10 were pro-carriers at codon 25.…”

Section: Tgf-␤1 Gene Polymorphismsmentioning

confidence: 95%

The Impact of Transforming Growth Factor-β1 Gene Polymorphism on End-Stage Renal Failure After Heart Transplantation

et al. 2006

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“…When TGF-b was directly injected into the subcutaneous tissue of newborn mice, accelerated fibrosis, that is, activation of fibroblasts to produce collagens, was demonstrated (Roberts et al, 1986;Shinozaki et al, 1997). In clinical diseases including pulmonary fibrosis and chronic renal allograft damage, TGF-b is also considered to be a main pathogenic factor for the overproduction of collagen (Nicholson et al, 1999). Obviously, TGF-b is not the only factor that can stimulate collagen expression in fibroblasts, since insulin and/or growth factors analysed here also regulate the production of type I collagen (Krupsky et al, 1996).…”

Section: Discussionmentioning

confidence: 99%

Overexpression of TGF-β by infiltrated granulocytes correlates with the expression of collagen mRNA in pancreatic cancer

et al. 2004

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Pancreatic cancer is often associated with an intense production of interstitial collagens, known as the desmoplastic reaction. To understand more about desmoplasia in pancreatic cancer, the expression of mRNA for type I and III collagens and potent desmoplastic inducing growth factors transforming growth factor-b (TGF-b), connective tissue growth factor (CTGF), acidic and basic fibroblast growth factor (FGF), platelet-derived growth factor (PDGF) A and C and epidermal growth factor (EGF) was analysed by quantitative RT-PCR. Expression of both collagens in 23 frozen primary pancreatic cancer nodules was significantly higher than that in 15 nonneoplastic pancreatic tissues. The expressions of mRNAs for TGF-b, acidic FGF, basic FGF and PDGF C were likewise higher in surgical cancer nodules, while that of CTGF, PDGF A and EGF were not. Among these growth factors, the expression of TGF-b mRNA showed the most significant correlation with that of collagens (Po0.0001). By immunohistochemistry, TGF-b showed faint cytoplasmic staining in cancer cells. In contrast, isolated cells, mainly located on the invasive front surrounding cancerous nests, were prominently and strongly stained. These TGF-b-positive cells contained a segmented nucleus, were negative for anti-macrophage (CD68) and positive for anti-granulocyte antibodies, indicating their granulocytic nature. In conclusion, TGF-b seemed to play a major role among the various growth factors in characteristic overproduction of collagens in pancreatic cancer. Moreover, the predominant cells that express TGF-b were likely to be infiltrated granulocytes (mostly are neutrophils) and not pancreatic cancer cells.

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“…Increased renal allograft expression of TGF-b also occurs in the clinical setting 98,99 . Nicholson et al 100 examined intragraft gene expression in glomeruli using a RT PCR and found a positive correlation between the level of glomerular complementary DNA for TGF-b and renal cortical collagen III immunostaining (P < 0´01). Intragraft TGF-b levels also correlate with a decline in allograft function.…”

Section: Angiotensin II Increases Ecm Deposition Via Tgf-b Induces Upmentioning

confidence: 99%

Molecular mechanisms of renal allograft fibrosis

Waller

Nicholson

2001

Journal of British Surgery

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Recent advances in understanding of the underlying molecular mechanisms involved suggest autocrine secretion of cytokines and growth factors, especially transforming growth factor beta, are associated with a change in fibroblast phenotype leading to the deposition of extracellular matrix. Repeated insults trigger upregulation of the tissue inhibitors of matrix metalloproteinases, favouring accumulation of extracellular matrix. To date, no drug has proved effective in inhibiting or reducing allograft fibrosis. The deleterious consequences of chronic immunosuppression on the development of such fibrosis are now recognized; newer immunosuppressive drugs, including rapamycin and mycophenolate mofetil, reduce profibrotic gene expression in both experimental and clinical settings, and offer potential strategies for prolonging allograft survival.

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Intragraft expression of transforming growth factor β1 gene in isolated glomeruli from human renal transplants

Abstract: TGF-beta1 is a profibrotic influence in human renal transplants. The methods described should prove of benefit in investigating the mechanisms of chronic renal allograft damage.

Cited by 15 publications

References 21 publications

The Impact of Transforming Growth Factor-β1 Gene Polymorphism on End-Stage Renal Failure After Heart Transplantation

The Impact of Transforming Growth Factor-β1 Gene Polymorphism on End-Stage Renal Failure After Heart Transplantation

Overexpression of TGF-β by infiltrated granulocytes correlates with the expression of collagen mRNA in pancreatic cancer

Molecular mechanisms of renal allograft fibrosis

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