Antifibrotic Effect of Smad Decoy Oligodeoxynucleotide in a CCl4-Induced Hepatic Fibrosis Animal Model
Hepatic fibrosis is the wound-healing process of chronic hepatic disease that leads to the end-stage of hepatocellular carcinoma and demolition of hepatic structures. Epithelial–mesenchymal transition (EMT) has been identified to phenotypic conversion of the epithelium to mesenchymal phenotype that...
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2018-08-01
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author | Mi-Gyeong Gwon Jung-Yeon Kim Hyun-Jin An Woon-Hae Kim Hyemin Gu Min-Kyung Kim Sok Cheon Pak Kwan-Kyu Park |
author_facet | Mi-Gyeong Gwon Jung-Yeon Kim Hyun-Jin An Woon-Hae Kim Hyemin Gu Min-Kyung Kim Sok Cheon Pak Kwan-Kyu Park |
author_sort | Mi-Gyeong Gwon |
collection | DOAJ |
description | Hepatic fibrosis is the wound-healing process of chronic hepatic disease that leads to the end-stage of hepatocellular carcinoma and demolition of hepatic structures. Epithelial–mesenchymal transition (EMT) has been identified to phenotypic conversion of the epithelium to mesenchymal phenotype that occurred during fibrosis. Smad decoy oligodeoxynucleotide (ODN) is a synthetic DNA fragment containing a complementary sequence of Smad transcription factor. Thus, this study evaluated the antifibrotic effects of Smad decoy ODN on carbon tetrachloride (CCl4)-induced hepatic fibrosis in mice. As shown in histological results, CCl4 treatment triggered hepatic fibrosis and increased Smad expression. On the contrary, Smad decoy ODN administration suppressed fibrogenesis and EMT process. The expression of Smad signaling and EMT-associated protein was markedly decreased in Smad decoy ODN-treated mice compared with CCl4-injured mice. In conclusion, these data indicate the practicability of Smad decoy ODN administration for preventing hepatic fibrosis and EMT processes. |
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spelling | doaj.art-c0f64ed56692485f9eaf7d5283cee4532022-12-21T18:48:25ZengMDPI AGMolecules1420-30492018-08-01238199110.3390/molecules23081991molecules23081991Antifibrotic Effect of Smad Decoy Oligodeoxynucleotide in a CCl4-Induced Hepatic Fibrosis Animal ModelMi-Gyeong Gwon0Jung-Yeon Kim1Hyun-Jin An2Woon-Hae Kim3Hyemin Gu4Min-Kyung Kim5Sok Cheon Pak6Kwan-Kyu Park7Department of Pathology, College of Medicine, Catholic University of Daegu, 33, Duryugongwon-ro 17-gil, Nam-gu, Daegu 42472, KoreaDepartment of Pathology, College of Medicine, Catholic University of Daegu, 33, Duryugongwon-ro 17-gil, Nam-gu, Daegu 42472, KoreaDepartment of Pathology, College of Medicine, Catholic University of Daegu, 33, Duryugongwon-ro 17-gil, Nam-gu, Daegu 42472, KoreaDepartment of Pathology, College of Medicine, Catholic University of Daegu, 33, Duryugongwon-ro 17-gil, Nam-gu, Daegu 42472, KoreaDepartment of Pathology, College of Medicine, Catholic University of Daegu, 33, Duryugongwon-ro 17-gil, Nam-gu, Daegu 42472, KoreaDepartment of Pathology, Dongguk University School of Medicine, Gyeongju 38066, KoreaSchool of Biomedical Sciences, Charles Sturt University, Panorama Avenue, Bathurst, NSW 2795, AustraliaDepartment of Pathology, College of Medicine, Catholic University of Daegu, 33, Duryugongwon-ro 17-gil, Nam-gu, Daegu 42472, KoreaHepatic fibrosis is the wound-healing process of chronic hepatic disease that leads to the end-stage of hepatocellular carcinoma and demolition of hepatic structures. Epithelial–mesenchymal transition (EMT) has been identified to phenotypic conversion of the epithelium to mesenchymal phenotype that occurred during fibrosis. Smad decoy oligodeoxynucleotide (ODN) is a synthetic DNA fragment containing a complementary sequence of Smad transcription factor. Thus, this study evaluated the antifibrotic effects of Smad decoy ODN on carbon tetrachloride (CCl4)-induced hepatic fibrosis in mice. As shown in histological results, CCl4 treatment triggered hepatic fibrosis and increased Smad expression. On the contrary, Smad decoy ODN administration suppressed fibrogenesis and EMT process. The expression of Smad signaling and EMT-associated protein was markedly decreased in Smad decoy ODN-treated mice compared with CCl4-injured mice. In conclusion, these data indicate the practicability of Smad decoy ODN administration for preventing hepatic fibrosis and EMT processes.http://www.mdpi.com/1420-3049/23/8/1991liver fibrosisSmaddecoyoligodeoxynucleotideCCl4 |
spellingShingle | Mi-Gyeong Gwon Jung-Yeon Kim Hyun-Jin An Woon-Hae Kim Hyemin Gu Min-Kyung Kim Sok Cheon Pak Kwan-Kyu Park Antifibrotic Effect of Smad Decoy Oligodeoxynucleotide in a CCl4-Induced Hepatic Fibrosis Animal Model Molecules liver fibrosis Smad decoy oligodeoxynucleotide CCl4 |
title | Antifibrotic Effect of Smad Decoy Oligodeoxynucleotide in a CCl4-Induced Hepatic Fibrosis Animal Model |
title_full | Antifibrotic Effect of Smad Decoy Oligodeoxynucleotide in a CCl4-Induced Hepatic Fibrosis Animal Model |
title_fullStr | Antifibrotic Effect of Smad Decoy Oligodeoxynucleotide in a CCl4-Induced Hepatic Fibrosis Animal Model |
title_full_unstemmed | Antifibrotic Effect of Smad Decoy Oligodeoxynucleotide in a CCl4-Induced Hepatic Fibrosis Animal Model |
title_short | Antifibrotic Effect of Smad Decoy Oligodeoxynucleotide in a CCl4-Induced Hepatic Fibrosis Animal Model |
title_sort | antifibrotic effect of smad decoy oligodeoxynucleotide in a ccl4 induced hepatic fibrosis animal model |
topic | liver fibrosis Smad decoy oligodeoxynucleotide CCl4 |
url | http://www.mdpi.com/1420-3049/23/8/1991 |
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