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פותח על ידי קלירמאש פתרונות בע"מ -
Inhibition of collagen type I synthesis by skin fibroblasts of graft versus host disease and scleroderma patients: Effect of halofuginone
Year:
1996
Source of publication :
Biochemical Pharmacology
Authors :
גנין, אולגה
;
.
פינס, מרק
;
.
Volume :
52
Co-Authors:
Halevy, O., Department of Animal Science, Faculty of Agriculture, Hebrew University of Jerusalem, Rehovot, Israel
Nagler, A., Dept. of Bone Marrow Transplantation, Hadassah University Hospital, Jerusalem, Israel
Levi-Schaffer, F., Department of Pharmacology, Hebrew University of Jerusalem, Jerusalem, Israel
Genina, O., Institute of Animal Science, Agricultural Research Organization, Volcani Center, Bet Dagan, Israel
Pines, M., Institute of Animal Science, Agricultural Research Organization, Volcani Center, Bet Dagan, Israel, Institute of Animal Science, Volcani Center, ARO, Bet Dagan 50250, Israel
Facilitators :
From page:
1057
To page:
1063
(
Total pages:
7
)
Abstract:
The effect of halofuginone (a plant alkaloid) on collagen α1(I) gene expression and collagen synthesis was evaluated in human skin fibroblasts from patients with chronic graft-versus-host disease (cGvHD) or scleroderma and from a normal individual. Halofuginone caused a dose-dependent inhibition in collagen α1(I) gene expression and collagen synthesis in all cultures tested, the cGvHD fibroblasts being the least sensitive. In normal and scleroderma fibroblasts, concentrations of halofuginone as low as 10-10 M and 10-9 M were sufficient to cause a significant reduction in collagen α1(I) gene expression and collagen synthesis, respectively. In addition, halofuginone also inhibited the transforming growth factor β-induced collagen synthesis. Three days after halofuginone removal, collagen gene expression returned to control levels. The reduction of collagen mRNA transcript levels by halofuginone appeared to be dependent on new protein synthesis because simultaneous treatment of fibroblasts with protein synthesis inhibitors prevents the suppressive effect of halofuginone on collagen α1(I) mRNA gene expression. The ability of extremely low concentrations of halofuginone to inhibit collagen α1(I) synthesis specifically and transiently at the transcriptional level suggests that this material may be an important tool for studying collagen α1(I) gene regulation and may be used as a novel and promising antifibrotic therapy.
Note:
Related Files :
adult
Autoimmunity
collagen α1(I)
Female
gene expression
Plant alkaloid
transforming growth factor beta
עוד תגיות
תוכן קשור
More details
DOI :
10.1016/0006-2952(96)00427-3
Article number:
Affiliations:
Database:
סקופוס
Publication Type:
מאמר
;
.
Language:
אנגלית
Editors' remarks:
ID:
26887
Last updated date:
02/03/2022 17:27
Creation date:
17/04/2018 00:26
Scientific Publication
Inhibition of collagen type I synthesis by skin fibroblasts of graft versus host disease and scleroderma patients: Effect of halofuginone
52
Halevy, O., Department of Animal Science, Faculty of Agriculture, Hebrew University of Jerusalem, Rehovot, Israel
Nagler, A., Dept. of Bone Marrow Transplantation, Hadassah University Hospital, Jerusalem, Israel
Levi-Schaffer, F., Department of Pharmacology, Hebrew University of Jerusalem, Jerusalem, Israel
Genina, O., Institute of Animal Science, Agricultural Research Organization, Volcani Center, Bet Dagan, Israel
Pines, M., Institute of Animal Science, Agricultural Research Organization, Volcani Center, Bet Dagan, Israel, Institute of Animal Science, Volcani Center, ARO, Bet Dagan 50250, Israel
Inhibition of collagen type I synthesis by skin fibroblasts of graft versus host disease and scleroderma patients: Effect of halofuginone
The effect of halofuginone (a plant alkaloid) on collagen α1(I) gene expression and collagen synthesis was evaluated in human skin fibroblasts from patients with chronic graft-versus-host disease (cGvHD) or scleroderma and from a normal individual. Halofuginone caused a dose-dependent inhibition in collagen α1(I) gene expression and collagen synthesis in all cultures tested, the cGvHD fibroblasts being the least sensitive. In normal and scleroderma fibroblasts, concentrations of halofuginone as low as 10-10 M and 10-9 M were sufficient to cause a significant reduction in collagen α1(I) gene expression and collagen synthesis, respectively. In addition, halofuginone also inhibited the transforming growth factor β-induced collagen synthesis. Three days after halofuginone removal, collagen gene expression returned to control levels. The reduction of collagen mRNA transcript levels by halofuginone appeared to be dependent on new protein synthesis because simultaneous treatment of fibroblasts with protein synthesis inhibitors prevents the suppressive effect of halofuginone on collagen α1(I) mRNA gene expression. The ability of extremely low concentrations of halofuginone to inhibit collagen α1(I) synthesis specifically and transiently at the transcriptional level suggests that this material may be an important tool for studying collagen α1(I) gene regulation and may be used as a novel and promising antifibrotic therapy.
Scientific Publication
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