Mannose-6-Phosphate/IGF-II Receptors Mediate the Effects of IGF-1-Induced Latent Transforming Growth Factor β1 on Expression of Type I Collagen and Collagenase in Dermal Fibroblasts

2000 ◽  
Vol 17 (3) ◽  
pp. 167-176 ◽  
Author(s):  
Aziz Ghahary ◽  
Edward E. Tredget ◽  
Qiong Shen ◽  
Ruhangiz T. Kilani ◽  
Paul G. Scott ◽  
...  
Keyword(s):  
Growth Factor ◽  
Type I Collagen ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Dermal Fibroblasts ◽  
Type I ◽  
Mannose 6 Phosphate

Synergetic Effect of Interleukin-4 and Transforming Growth Factor-β1 on Type I Collagen Gel Contraction and Degradation by HFL-1 Cells

CHEST Journal ◽  
2003 ◽  
Vol 123 (3) ◽  
pp. 427S-428S ◽  
Author(s):  
Xiangde Liu ◽  
Heather Conner ◽  
Tetsu Kobayashi ◽  
Shinji Abe ◽  
Qiuhong Fang ◽  
...  
Keyword(s):  
Growth Factor ◽  
Type I Collagen ◽  
Transforming Growth Factor ◽  
Synergetic Effect ◽  
Collagen Gel ◽  
Transforming Growth Factor Β1 ◽  
Interleukin 4 ◽  
Type I ◽  
Collagen Gel Contraction ◽  
Type I Collagen Gel

scholarly journals Leukoregulin down-regulates type I collagen mRNA levels and promoter activity in human dermal fibroblasts, and counteracts the up-regulation elicited by transforming growth factor-β

1992 ◽  
Vol 284 (3) ◽  
pp. 629-632 ◽  
Author(s):  
A Mauviel ◽  
C H Evans ◽  
J Uitto
Keyword(s):  
Gene Expression ◽  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Promoter Activity ◽  
Type I Collagen ◽  
Transforming Growth Factor ◽  
Dermal Fibroblasts ◽  
Type I ◽  
Mrna Levels ◽  
Human Dermal Fibroblasts

Leukoregulin (LR), a T-cell-derived growth factor, modulates fibroblast functions in vitro [Mauviel, Rédini, Hartmann, Loyau & Pujol (1991) J. Cell Biol. 113, 1455-1462]. In the present study, incubation of human dermal fibroblasts with LR (0.1-2 units/ml) resulted in decreases in the mRNA steady-state levels for alpha 1(I), alpha 2(I) and alpha 1(III), but not alpha 2(V), collagen genes. LR also down-regulated alpha 2(I) collagen promoter activity in transient cell transfections of control cells as well as those incubated with transforming growth factor-beta, a potent up-regulator of collagen type I gene expression. Thus LR is a strong inhibitor of type I collagen gene expression, acting at the level of transcription.

scholarly journals Decreased MiR-30a promotes TGF-β1-mediated arachnoid fibrosis in post-hemorrhagic hydrocephalus

2020 ◽  
Vol 11 (1) ◽  
pp. 60-74
Author(s):  
Chaohong Zhan ◽  
Gelei Xiao ◽  
Xiangyang Zhang ◽  
Xiaoyu Chen ◽  
Zhiping Zhang ◽  
...  
Keyword(s):  
Growth Factor ◽  
Intraventricular Hemorrhage ◽  
Type I Collagen ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Ventricular System ◽  
Type I ◽  
Cerebral Ventricles ◽  
The Right ◽  
Tgf Β1

AbstractBackgroundFibrosis in the ventricular system is closely associated with post-hemorrhagic hydrocephalus (PHH). It is characterized by an expansion of the cerebral ventricles due to CSF accumulation following intraventricular hemorrhage (IVH). The activation of transforming growth factor-β1 (TGF-β1) may be involved in thrombin-induced arachnoid fibrosis.MethodsA rat model of PHH was established by injection of autologous non-anticoagulated blood from the right femoral artery into the lateral ventricles. Differential expression of miR-30a was detected in rat arachnoid cells by RNA sequencing. AP-1, c-Fos, and TRAF3IP2 were knocked down in primary arachnoid cells, and the degree of arachnoid fibrosis was assessed.ResultsDecreased expression of miR-30a and increased expression of TRAF3IP2, TGF-β1, and α-SMA were detected in the arachnoid cells of PHH rat. Besides, overexpression of miR-30a targets TRAF3IP2 mRNA 3′UTR and inhibits the expression of TRAF3IP2, TGF-β1, and α-SMA in the primary arachnoid cells. Furthermore, TRAF3IP2 activates AP-1 to promote arachnoid fibrosis. The content of type I collagen in the primary arachnoid cells was reduced after the silencing of AP-1 and TRAF3IP2.ConclusionsThis study identified a miR-30a-regulated mechanism of arachnoid fibrosis, suggesting a previously unrecognized contribution of miR-30a to the pathogenesis of fibrosis in the ventricular system. These results might provide a new target for the clinical diagnosis and treatment of PHH.

Stress-relaxation and contraction of a collagen matrix induces expression of TGF-β and triggers apoptosis in dermal fibroblasts

2000 ◽  
Vol 78 (4) ◽  
pp. 427-436 ◽  
Author(s):  
M Varedi ◽  
E E Tredget ◽  
A Ghahary ◽  
P G Scott
Keyword(s):  
Mechanical Properties ◽  
Growth Factor ◽  
Type I Collagen ◽  
Transforming Growth Factor ◽  
Collagen Matrix ◽  
Dermal Fibroblasts ◽  
Type I ◽  
Collagen Matrices ◽  
Matrix Metalloproteinase 1 ◽  
Tgf Β1

Extracellular matrix serves as a scaffold for cells and can also regulate gene expression and ultimately cell behaviour. In this study, we compared the effects of three forms of type I collagen matrix, which differed only in their mechanical properties, and plastic on the expression of transforming growth factor-β1 (TGF-β1), matrix metalloproteinase-1 (collagenase), and type I collagen and on the growth and survival of human dermal fibroblasts. These effects were correlated with alterations in cell morphology and organization of intracellular actin. Cells in detached or stress-relaxed matrices were spherical, lacked stress fibres, and showed increased TGF-β1 mRNA compared to the cells in anchored collagen matrices or on plastic, which were polygonal or bipolar and formed stress fibres. The levels of TGF-β measured by bioassay were higher in detached and stress-relaxed collagen matrices, than in anchored collagen matrices. Cells on plastic contained little or no immunoreactive TGF-β, while most cells in collagen matrices were stained. The levels of collagenase mRNA were significantly higher in all the collagen matrix cultures compared to those on plastic, but there were no statistically significant differences between them. Levels of mRNA for procollagen type I were not significantly affected by culture in the collagen matrices. Apoptotic fibroblasts were detected by the TUNEL assay in detached (5.7%) and to a lesser extent in stress-relaxed (2.2%) matrices, but none were observed in anchored collagen matrices or on plastic. These results show that alterations in the mechanical properties of matrix can induce the expression of TGF-β and trigger apoptosis in dermal fibroblasts. They further suggest that inability to reorganize this matrix could be responsible for the maintenance of the fibroproliferative phenotype associated with fibroblasts in hypertrophic scarring. Key words: transforming growth factor-β, apoptosis, fibroblasts.

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