scholarly journals ALTERATION IN GENE EXPRESSION OF TRANSFORMING GROWTH FACTOR- Β FOLLOWING TREATMENT OF HYPERTROPHIC BURN SCARS WITH THREE DIFFERENT THERAPEUTIC MODALITIES

2019 ◽  
Vol 3 (7) ◽  
Author(s):  
Vaibhav Jain ◽  
Jyoti Gupta ◽  
Neeraj Gupta ◽  
Pradeep Jain
Keyword(s):  
Growth Factor ◽  
Hypertrophic Scar ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Tgf Beta ◽  
Burn Scar ◽  
Therapeutic Modalities ◽  
Silicone Gel ◽  
Triamcinolone Injection ◽  
Silicone Gel Sheet

Background: Hypertrophic scar (HTS) is a dermal form of fibro-proliferative disorder often caused by thermal injury to the deep dermis. Transforming growth factor β1 & 2 are well known pro-fibrotic cytokines promoting ECM production and tissue fibrosis. The present study was designed to evaluate the different therapeutic modalities for management of hypertrophic scar and correlate it with altered expression of TGF beta gene at the molecular level. Materials and Methods: One hundred and twenty patients with hypertrophic post burn scar were randomly distributed into three different treatment groups of Pressure Garments, Silicone Gel Sheet and Triamcinolone Injection. Total RNA was isolated from the scar tissue in cases before and 6 months after the therapy and from normal skin in controls to evaluate the expression of TGF beta (1, 2 & 3) by real time PCR. Results: Following treatment, the expression of TGF β-1 & 2 was down regulated while that of β-3 up regulated. The overall positive response (combining all the groups) was 94% out of which, 16.6% were cured, 47.5% showed major improvement and minor changes were observed in 30.8% of patients. Discussion: All the three modalities of treatment were effective in bringing down the level of TGF β-1&2 and in up-regulating antifibrotic β3 and this correlated well with the clinical improvement in the scar thickness, pliability etc. Conclusion: Out of all, intralesional Triamcinolone Injection achieved the best result. Keywords: Hypertrophic Scar, Transforming Growth Factor β, Pressure Garments, Silicone Gel Sheet, Triamcinolone Injection

scholarly journals Phosphorylation of the human-transforming-growth-factor-β-binding protein endoglin

1994 ◽  
Vol 301 (3) ◽  
pp. 765-768 ◽  
Author(s):  
P Lastres ◽  
J Martín-Perez ◽  
C Langa ◽  
C Bernabéu
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Mouse Fibroblast ◽  
Tgf Beta ◽  
Kinase C ◽  
Protein Kinase C Inhibitor ◽  
A Minor ◽  
Minor Extent

Endoglin is an homodimeric membrane antigen with capacity to bind transforming growth factor-beta (TGF-beta). Phosphorylation of human endoglin was demonstrated in endothelial cells as well as in mouse fibroblast transfectants expressing two isoforms, L-endoglin or S-endoglin, with distinct cytoplasmic domains. The extent of L-endoglin phosphorylation was found to be 8-fold higher than that of S-endoglin, and phosphopeptide analyses revealed at least three different phosphorylation sites for L-endoglin, whereas S-endoglin produces only one phosphopeptide. The immunoprecipitated L-endoglin was found to be phosphorylated mainly on serine, and, to a minor extent, on threonine, residues. Treatment of the cells with TGF-beta 1 or the protein kinase C inhibitor H-7 resulted in a reduction of the levels of endoglin phosphorylation.

Modulation of Collagen Synthesis by Transforming Growth Factor-β in Keloid and Hypertrophic Scar Fibroblasts

1994 ◽  
Vol 33 (2) ◽  
pp. 148-154 ◽  
Author(s):  
Soheil Younai ◽  
Larry S. Nichter ◽  
Tadeusz Wellisz ◽  
John Reinisch ◽  
Marcel E. Nimni ◽  
...  
Keyword(s):  
Growth Factor ◽  
Hypertrophic Scar ◽  
Collagen Synthesis ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β

scholarly journals Inhibition of Nb2 T-lymphoma cell growth by transforming growth factor-β

1988 ◽  
Vol 253 (1) ◽  
pp. 295-298 ◽  
Author(s):  
E J Rayhel ◽  
D A Prentice ◽  
P S Tabor ◽  
W H Flurkey ◽  
R W Geib ◽  
...  
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Interleukin 2 ◽  
Transforming Growth Factor Β ◽  
Tgf Beta ◽  
Inhibitory Effects ◽  
Nb2 Cells ◽  
Growth Factor Beta ◽  
T Lymphoma

Transforming growth factor-beta (TGF-beta) inhibits proliferation of Nb2 cells, a rat T lymphoma, in response to lactogens and interleukin-2. Prostaglandins may play an important role in the pathway through which TGF-beta exerts its inhibitory actions, because prostaglandin E2 also inhibits proliferation of Nb2 cells, and indomethacin, an inhibitor of prostaglandin synthesis, reverses the inhibitory effects of TGF-beta on Nb2 cell proliferation.

scholarly journals Non-uniform influence of transforming growth factor-β on the biosynthesis of different forms of small chondroitin sulphate/dermatan sulphate proteoglycan

1990 ◽  
Vol 269 (2) ◽  
pp. 551-554 ◽  
Author(s):  
B Breuer ◽  
G Schmidt ◽  
H Kresse
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Core Protein ◽  
Chondroitin Sulphate ◽  
Transforming Growth Factor Β ◽  
Cell Types ◽  
Osteosarcoma Cell ◽  
Tgf Beta ◽  
Small Proteoglycan

The influence of transforming growth factor-beta (TGF-beta) on the expression of different forms of small proteoglycans was investigated in human skin fibroblasts and in a human osteosarcoma cell line. TGF-beta was not found to act as a general stimulator of small proteoglycan biosynthesis. In both cell types, an increased expression of the core protein of proteoglycan I was found. However, there was a profound decrease in the expression of a 106 kDa core protein, and either no alteration or a small decrease in the biosynthesis of the collagen-binding small proteoglycan II core protein. These results show that the production of individual members of the small proteoglycan family is differentially regulated.

scholarly journals Editorial Special Issue TGF-Beta/BMP Signaling Pathway

Cells ◽  
2020 ◽  
Vol 9 (11) ◽  
pp. 2363
Author(s):  
Isabel Fabregat ◽  
Blanca Herrera ◽  
Aránzazu Sánchez
Keyword(s):  
Growth Factor ◽  
Signaling Pathway ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Bmp Signaling ◽  
Tissue Homeostasis ◽  
Tgf Beta ◽  
Special Issue ◽  
Editorial Special Issue

The transforming growth factor β (TGF-β) superfamily plays key roles in development and tissue homeostasis, controlling the maintenance and regeneration of mature tissues [...]

scholarly journals Transforming-growth-factor-β activation elements in the distal promoter regions of the rat α1 type I collagen gene

1991 ◽  
Vol 280 (1) ◽  
pp. 157-162 ◽  
Author(s):  
J D Ritzenthaler ◽  
R H Goldstein ◽  
A Fine ◽  
A Lichtler ◽  
D W Rowe ◽  
...  
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Transcriptional Activation ◽  
Type I Collagen ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Collagen Type I ◽  
Type I ◽  
Tgf Beta ◽  
Mobility Shift

We have located a cis-acting element (alpha 1-TAE) within the promoter sequences of the rat collagen alpha 1(I) gene (COL1A1) 1600 bases upstream of the transcription start site which mediates transcriptional activation by transforming growth factor beta (TGF-beta). The functional significance of this region was established by (1) deletion analysis of the alpha 1(I) promoter cloned upstream of the bacterial chloramphenicol acetyltransferase (CAT) gene and (2) by co-transfection of promoter constructs with double-stranded oligonucleotides. DNA-mobility-shift assays with radiolabelled alpha 1-TAE demonstrated increased nuclear binding activity after TGF-beta stimulation. Oligonucleotides encoding the alpha 1-TAE, additional upstream regions within the alpha 1(I) promoter, as well as consensus nuclear-factor-1 (NF-1) sequences, competed with the alpha 1-TAE sequence. The two collagen type I genes are stimulated by TGF-beta through different regions of their promoters.

scholarly journals Collagen synthesis by human fibroblasts. Regulation by transforming growth factor-β in the presence of other inflammatory mediators

1989 ◽  
Vol 260 (2) ◽  
pp. 463-469 ◽  
Author(s):  
A S Narayanan ◽  
R C Page ◽  
J Swanson
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Collagen Synthesis ◽  
Transforming Growth Factor ◽  
Human Fibroblasts ◽  
Transforming Growth Factor Β ◽  
Tgf Beta ◽  
Collagen Production ◽  
Collagen Mrna ◽  
In Cells

We have examined the combined effects of transforming growth factor-beta (TGF-beta), serum and gamma-interferon (gamma-IFN) on collagen synthesis by fibroblasts and compared the response of fibroblast subpopulations to TGF-beta. Human diploid fibroblasts were treated with TGF-beta alone and with serum of gamma-IFN. Cells were labelled with radioactive amino acids, and collagen production was measured as collagenase-digestible radioactivity. Collagen mRNA was determined by a solution-hybridization assay using procollagen-alpha 1[I] cDNA clone HF 677. The results showed that either serum or TGF-beta increased incorporation, collagen production and mRNA by fibroblasts approx. 2-fold; however, collagen synthesis relative to total protein synthesis and collagen mRNA relative to total polyadenylated [poly(A)+] RNA were not affected. Only serum activated cell growth. Collagen production increased approx. 4-fold in cells exposed to both TGF-beta and serum, and this increase was equal to that expected for an additive effect by both components. Treatment with gamma-IFN decreased collagen production and collagen mRNA to 44 and 40% respectively, whereas total incorporation and poly(A)+ RNA were affected only marginally. Cells exposed simultaneously to both gamma-IFN and TGF-beta produced less collagen and contained less mRNA than did those treated with TGF-beta alone. The gamma-IFN decreased collagen synthesis in control and TGF-beta-treated cultures to a similar extent, and TGF-beta increased collagen synthesis 2-fold in cells pre-treated with gamma-IFN. Fibroblast strains obtained in medium containing plasma-derived serum synthesized approximately half as much collagen as did cells derived from the same explant in the presence of fresh human serum, and TGF-beta stimulated collagen production and mRNA in both cell strains. We conclude that TGF-beta, serum and gamma-IFN regulate collagen synthesis by independent mechanisms, and that the combined action of these components plays a significant role in regulating collagen synthesis during wound healing and tissue repair.

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