Glucose-induced fibronectin and collagen type III expression in renal fibroblasts can occur independent of TGF-β1

Lam, Suzanne; Verhagen, Nicole A.M.; Strutz, Frank; Pijl, J.W. van der; Daha, Mohamed R.; Kooten, Cees van

doi:10.1046/j.1523-1755.2003.00824.x

Cited by 38 publications

(32 citation statements)

References 42 publications

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“…In addition, TK173-⌬T␤RII was exposed to either TGF-␤1 or high glucose. We recently demonstrated that glucose-induced collagen type III was not affected in these transfected cells (8). Now we also show that collagen type I secretion induced by high glucose was not affected in TK173-⌬T␤RII, whereas the effect of TGF-␤1 was completely abolished (Fig.…”

Section: Resultssupporting

confidence: 67%

“…Recently, we demonstrated a TGF-␤1-independent mechanism of fibronectin and collagen type III upregulation in human renal fibroblasts by high glucose, in a process that might involve alternative growth factors (8).…”

Section: Discussionmentioning

confidence: 99%

“…Collagen type I and III accumulation in supernatants was measured using a specific inhibition ELISA as previously described (8). Briefly, 96-well Nunc Maxisorb microtiter plates (Gibco/Invitrogen) were coated with 0.5 g/ml human collagen type I or III (both purchased from Sigma) in PBS (100 l/well) overnight at room temperature.…”

Section: Methodsmentioning

confidence: 99%

“…Recently, we demonstrated that TGF-␤1 is not required for glucose-induced ECM accumulation in human renal fibroblasts, a process that might involve alternative growth factors (8). Moreover, collagen type III was not affected by TGF-␤1, suggesting that the growth factor requirement for the induction of collagen type III is different from other ECM components.…”

mentioning

confidence: 90%

“…Recently, we demonstrated in vitro that TGF-␤1 was not required for glucose-induced ECM accumulation in renal fibroblasts, in a process that might involve alternative growth factors (8). Moreover, other growth factors have been implicated in vivo to contribute to the pathogenesis of diabetic nephropathy (9 -11).…”

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confidence: 99%

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Connective Tissue Growth Factor and IGF-I Are Produced by Human Renal Fibroblasts and Cooperate in the Induction of Collagen Production by High Glucose

et al. 2003

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Tubulointerstitial fibrosis is an important component in the development of diabetic nephropathy. Various renal cell types, including fibroblasts, contribute to the excessive matrix deposition in the kidney. Although transforming growth factor-␤ (TGF-␤) has been thought to play a major role during fibrosis, other growth factors are also involved. Here we examined the effects of connective tissue growth factor (CTGF) and IGF-I on collagen type I and III production by human renal fibroblasts and their involvement in glucose-induced matrix accumulation. We have demonstrated that both CTGF and IGF-I expressions were increased in renal fibroblasts under hyperglycemic conditions, also in the absence of TGF-␤ signaling. Although CTGF alone had no effect on collagen secretion, combined stimulation with IGF-I enhanced collagen accumulation. Furthermore, IGF-I also had a synergistic effect with glucose on the induction of collagens. Moreover, we observed a partial inhibition in glucose-induced collagen secretion with neutralizing anti-CTGF antibodies, thereby demonstrating for the first time the involvement of endogenous CTGF in glucose-induced effects in human renal fibroblasts. Therefore, the cooperation between CTGF and IGF-I might be involved in glucose-induced matrix accumulation in tubulointerstitial fibrosis and might contribute to the pathogenesis of diabetic nephropathy.

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Section: Resultssupporting

confidence: 67%

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 90%

mentioning

confidence: 99%

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Connective Tissue Growth Factor and IGF-I Are Produced by Human Renal Fibroblasts and Cooperate in the Induction of Collagen Production by High Glucose

et al. 2003

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TGF‐β1 drives partial myofibroblastic differentiation in chondromyxoid fibroma of bone

Romeo

Eyden

Prins

et al. 2005

The Journal of Pathology

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Chondromyxoid fibroma (CMF) is a rare benign cartilaginous bone tumour with a lobular architecture containing stellate and myofibroblast-like spindle cells. The aim of this study was to investigate the presence, spatial distribution, and extent of myoid differentiation in CMF and to evaluate a possible causative role for TGF-beta1 signalling, which is known to promote smooth muscle actin (SMA) expression. Twenty cases were studied for immunoreactivity for muscle-specific actin (MSA), SMA, desmin, h-caldesmon, calponin, TGF-beta1, and plasminogen activator inhibitor type 1 (PAI-1). The extent of myofibroblastic differentiation was further investigated ultrastructurally, including immuno-electron microscopy using antibodies against MSA and SMA, focusing upon the different cell types in CMF. The expression of potential genes driving this process was quantified by Q-RT-PCR (TGF-beta1, fibronectin, its EDA splice variant, and PAI-1). Tumour cells, especially those with a spindled morphology, showed diffuse immunoreactivity for MSA, SMA, TGF-beta1, and PAI-1, while desmin, h-caldesmon, and calponin were absent. Ultrastructurally, neoplastic cells showed the presence of myofilaments and rare dense bodies, which were more prominent in spindle cells and less so in chondroblast-like cells. Immuno-electron microscopy confirmed the actin nature of these myofilaments. No fibronexus was identified. The functional activity of TGF-beta1 was demonstrated by the identification of PAI-1, a related downstream molecule both immunohistochemically as well as by Q-RT-PCR. There was a linear correlation between TGF-beta1 and PAI-1 expression. Fibronectin-EDA levels were low. We have therefore substantiated the presence of morphological, immunohistochemical, and immuno-electron microscopic partial myofibroblastic differentiation in CMF, driven by TGF-beta1 signalling.

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The role of promoter hypermethylation in fibroblast activation and fibrogenesis

Zeisberg

2012

The Journal of Pathology

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The aberrant methylation of CpG island promoters of selected genes is the prominent epigenetic mechanism by which gene transcription can be effectively silenced. Aberrant hypermethylation of a few selected genes plays an important role in facilitating fibrotic fibroblast activation and in driving fibrogenesis. Here we review mechanisms of DNA methylation and demethylation and their implications for fibroblast activation and tissue fibrosis.

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Glucose-induced fibronectin and collagen type III expression in renal fibroblasts can occur independent of TGF-β1

Cited by 38 publications

References 42 publications

Connective Tissue Growth Factor and IGF-I Are Produced by Human Renal Fibroblasts and Cooperate in the Induction of Collagen Production by High Glucose

Connective Tissue Growth Factor and IGF-I Are Produced by Human Renal Fibroblasts and Cooperate in the Induction of Collagen Production by High Glucose

TGF‐β1 drives partial myofibroblastic differentiation in chondromyxoid fibroma of bone

The role of promoter hypermethylation in fibroblast activation and fibrogenesis

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