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פותח על ידי קלירמאש פתרונות בע"מ -
Inhibition of glomerular mesangial cell proliferation and extracellular matrix deposition by halofuginone
Year:
1997
Source of publication :
Kidney International
Authors :
גנין, אולגה
;
.
פינס, מרק
;
.
Volume :
52
Co-Authors:
Nagler, A.
Katz, A.
Aingorn, H.
Miao, H.-Q.
Condiotti, R.
Genina, O.
Pines, M.
Vlodavsky, I., Department of Oncology, Hadassah Hospital, P.O. Box 12000, Jerusalem, 91120, Israel
Facilitators :
From page:
1561
To page:
1569
(
Total pages:
9
)
Abstract:
Mesangial cell proliferation, increased deposition of collagen, and expansion of the mesangial extracellular matrix (ECM) are key features in the development of mesangioproliferative diseases. Halofuginone, a low molecular weight anti-coccidial quinoazolinone derivative, inhibits collagen type αl(I) gene expression and synthesis. We investigated the effect of halofuginone on both normal and SV40 transformed mesangial cell proliferation, collagen synthesis, and ECM deposition. Proliferation of both cell types was almost completely inhibited in the presence of 50 ng/ml halofuginone. The cells were arrested in the late G1 phase of the cell cycle and resumed their normal growth rate following removal of the compound from the culture medium. The antiproliferative effect of halofuginone was associated with inhibition of tyrosine phosphorylation of cellular proteins. Similar results were obtained whether the mesangial cells were seeded on regular tissue culture plastic or in close contact with a naturally produced ECM resembling their local environment in vivo. Halofuginone also inhibited synthesis and deposition of ECM by mesangial cells as indicated by a substantial reduction in 14C-glycine and Na235SO4 incorporation into the ECM, and by the inhibition of collagen type I synthesis and gene expression. It is proposed that by inhibiting collagen type I synthesis and matrix deposition, halofuginone exerts a potent antiproliferative effect that may he applied to inhibit mesangial cell proliferation and matrix expansion in a variety of chronic progressive glomerular diseases.
Note:
Related Files :
animal cell
Animals
cell cycle G1 phase
Cell Division
Cell Proliferation
drug effect
gene expression
Sulfates
tritium
עוד תגיות
תוכן קשור
More details
DOI :
Article number:
Affiliations:
Database:
סקופוס
Publication Type:
מאמר
;
.
Language:
אנגלית
Editors' remarks:
ID:
20231
Last updated date:
02/03/2022 17:27
Creation date:
16/04/2018 23:35
Scientific Publication
Inhibition of glomerular mesangial cell proliferation and extracellular matrix deposition by halofuginone
52
Nagler, A.
Katz, A.
Aingorn, H.
Miao, H.-Q.
Condiotti, R.
Genina, O.
Pines, M.
Vlodavsky, I., Department of Oncology, Hadassah Hospital, P.O. Box 12000, Jerusalem, 91120, Israel
Inhibition of glomerular mesangial cell proliferation and extracellular matrix deposition by halofuginone
Mesangial cell proliferation, increased deposition of collagen, and expansion of the mesangial extracellular matrix (ECM) are key features in the development of mesangioproliferative diseases. Halofuginone, a low molecular weight anti-coccidial quinoazolinone derivative, inhibits collagen type αl(I) gene expression and synthesis. We investigated the effect of halofuginone on both normal and SV40 transformed mesangial cell proliferation, collagen synthesis, and ECM deposition. Proliferation of both cell types was almost completely inhibited in the presence of 50 ng/ml halofuginone. The cells were arrested in the late G1 phase of the cell cycle and resumed their normal growth rate following removal of the compound from the culture medium. The antiproliferative effect of halofuginone was associated with inhibition of tyrosine phosphorylation of cellular proteins. Similar results were obtained whether the mesangial cells were seeded on regular tissue culture plastic or in close contact with a naturally produced ECM resembling their local environment in vivo. Halofuginone also inhibited synthesis and deposition of ECM by mesangial cells as indicated by a substantial reduction in 14C-glycine and Na235SO4 incorporation into the ECM, and by the inhibition of collagen type I synthesis and gene expression. It is proposed that by inhibiting collagen type I synthesis and matrix deposition, halofuginone exerts a potent antiproliferative effect that may he applied to inhibit mesangial cell proliferation and matrix expansion in a variety of chronic progressive glomerular diseases.
Scientific Publication
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