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פותח על ידי קלירמאש פתרונות בע"מ -
The role of iNOS in cholesterol-induced liver fibrosis
Year:
2015
Source of publication :
Laboratory Investigation
Authors :
גנין, אולגה
;
.
פינס, מרק
;
.
Volume :
95
Co-Authors:
Anavi, S., Institute of Biochemistry, Food Science and Nutrition, Robert H. Smith Faculty of Agriculture, Food and Environment, Hebrew University of Jerusalem, PO Box 12, Rehovot, Israel
Eisenberg-Bord, M., Institute of Biochemistry, Food Science and Nutrition, Robert H. Smith Faculty of Agriculture, Food and Environment, Hebrew University of Jerusalem, PO Box 12, Rehovot, Israel
Hahn-Obercyger, M., Institute of Biochemistry, Food Science and Nutrition, Robert H. Smith Faculty of Agriculture, Food and Environment, Hebrew University of Jerusalem, PO Box 12, Rehovot, Israel
Genin, O., Institute of Animal Sciences, Volcani Center, Bet Dagan, Israel
Pines, M., Institute of Animal Sciences, Volcani Center, Bet Dagan, Israel
Tirosh, O., Institute of Biochemistry, Food Science and Nutrition, Robert H. Smith Faculty of Agriculture, Food and Environment, Hebrew University of Jerusalem, PO Box 12, Rehovot, Israel
Facilitators :
From page:
914
To page:
924
(
Total pages:
11
)
Abstract:
Accumulation of cholesterol in the liver is associated with the development of non-alcoholic steatohepatitis-related fibrosis. However, underlying mechanisms are not well understood. The present study investigated the role of inducible nitric oxide synthase (iNOS) in cholesterol-induced liver fibrosis by feeding wild-type (WT) and iNOS-deficient mice with control or high-cholesterol diet (HCD) for 6 weeks. WT mice fed with HCD developed greater liver fibrosis, compared with iNOS-deficient mice, as evident by Sirius red staining and higher expression levels of profibrotic genes. Enhanced liver fibrosis in the presence of iNOS was associated with hypoxia-inducible factor-1α stabilization, matrix metalloproteinase-9 expression, and enhanced hepatic DNA damage. The profibrotic role of iNOS was also demonstrated in vivo using a selective inhibitor of iNOS as well as in vitro in a rat liver stellate cell line (HSC-T6). In conclusion, these findings suggest that iNOS is an important mediator in HCD-induced liver fibrosis. © 2015 USCAP, Inc All rights reserved.
Note:
Related Files :
adult
Animal
animal experiment
Animals
gene expression
Genetics
Male
metabolism
mice
Pathology
עוד תגיות
תוכן קשור
More details
DOI :
10.1038/labinvest.2015.67
Article number:
Affiliations:
Database:
סקופוס
Publication Type:
מאמר
;
.
Language:
אנגלית
Editors' remarks:
ID:
26927
Last updated date:
02/03/2022 17:27
Creation date:
17/04/2018 00:26
You may also be interested in
Scientific Publication
The role of iNOS in cholesterol-induced liver fibrosis
95
Anavi, S., Institute of Biochemistry, Food Science and Nutrition, Robert H. Smith Faculty of Agriculture, Food and Environment, Hebrew University of Jerusalem, PO Box 12, Rehovot, Israel
Eisenberg-Bord, M., Institute of Biochemistry, Food Science and Nutrition, Robert H. Smith Faculty of Agriculture, Food and Environment, Hebrew University of Jerusalem, PO Box 12, Rehovot, Israel
Hahn-Obercyger, M., Institute of Biochemistry, Food Science and Nutrition, Robert H. Smith Faculty of Agriculture, Food and Environment, Hebrew University of Jerusalem, PO Box 12, Rehovot, Israel
Genin, O., Institute of Animal Sciences, Volcani Center, Bet Dagan, Israel
Pines, M., Institute of Animal Sciences, Volcani Center, Bet Dagan, Israel
Tirosh, O., Institute of Biochemistry, Food Science and Nutrition, Robert H. Smith Faculty of Agriculture, Food and Environment, Hebrew University of Jerusalem, PO Box 12, Rehovot, Israel
The role of iNOS in cholesterol-induced liver fibrosis
Accumulation of cholesterol in the liver is associated with the development of non-alcoholic steatohepatitis-related fibrosis. However, underlying mechanisms are not well understood. The present study investigated the role of inducible nitric oxide synthase (iNOS) in cholesterol-induced liver fibrosis by feeding wild-type (WT) and iNOS-deficient mice with control or high-cholesterol diet (HCD) for 6 weeks. WT mice fed with HCD developed greater liver fibrosis, compared with iNOS-deficient mice, as evident by Sirius red staining and higher expression levels of profibrotic genes. Enhanced liver fibrosis in the presence of iNOS was associated with hypoxia-inducible factor-1α stabilization, matrix metalloproteinase-9 expression, and enhanced hepatic DNA damage. The profibrotic role of iNOS was also demonstrated in vivo using a selective inhibitor of iNOS as well as in vitro in a rat liver stellate cell line (HSC-T6). In conclusion, these findings suggest that iNOS is an important mediator in HCD-induced liver fibrosis. © 2015 USCAP, Inc All rights reserved.
Scientific Publication
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