Alcohol dehydrogenase III exacerbates liver fibrosis by enhancing stellate cell activation and suppressing natural killer cells in mice

The important roles of retinols and their metabolites have recently been emphasized in the interactions between hepatic stellate cells (HSCs) and natural killer (NK) cells. Nevertheless, the expression and role of retinol metabolizing enzyme in both cell types have yet to be clarified. Thus, we inve...

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Published in:Hepatology (Baltimore, Md.) Md.), 2014-09, Vol.60 (3), p.1044-1053
Main Authors: Yi, Hyon‐Seung, Lee, Young‐Sun, Byun, Jin‐Seok, Seo, Wonhyo, Jeong, Jong‐Min, Park, Ogyi, Duester, Gregg, Haseba, Takeshi, Kim, Sun Chang, Park, Keun‐Gyu, Gao, Bin, Jeong, Won‐Il
Format: Article
Language:English
Subjects:
Alcohol
Aldehyde Oxidoreductases - metabolism
Animals
Bone Marrow Transplantation
Dehydrogenases
Enzymes
Gene expression
Hepatic Stellate Cells - physiology
Hepatology
Immune system
Interferon-gamma - metabolism
Killer Cells, Natural - physiology
Liver cirrhosis
Liver Cirrhosis - enzymology
Liver Cirrhosis - immunology
Male
Mice
Mice, Inbred C57BL
Rodents
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creator Yi, Hyon‐Seung
Lee, Young‐Sun
Byun, Jin‐Seok
Seo, Wonhyo
Jeong, Jong‐Min
Park, Ogyi
Duester, Gregg
Haseba, Takeshi
Kim, Sun Chang
Park, Keun‐Gyu
Gao, Bin
Jeong, Won‐Il
description The important roles of retinols and their metabolites have recently been emphasized in the interactions between hepatic stellate cells (HSCs) and natural killer (NK) cells. Nevertheless, the expression and role of retinol metabolizing enzyme in both cell types have yet to be clarified. Thus, we investigated the expression of retinol metabolizing enzyme and its role in liver fibrosis. Among several retinol metabolizing enzymes, only alcohol dehydrogenase (ADH) 3 expression was detected in isolated HSCs and NK cells, whereas hepatocytes express all of them. In vitro treatment with 4‐methylpyrazole (4‐MP), a broad ADH inhibitor, or depletion of the ADH3 gene down‐regulated collagen and transforming growth factor‐β1 (TGF‐β1) gene expression, but did not affect α‐smooth muscle actin gene expression in cultured HSCs. Additionally, in vitro, treatments with retinol suppressed NK cell activities, whereas inhibition of ADH3 enhanced interferon‐γ (IFN‐γ) production and cytotoxicity of NK cells against HSCs. In vivo, genetic depletion of the ADH3 gene ameliorated bile duct ligation‐ and carbon tetrachloride‐induced liver fibrosis, in which a higher number of apoptotic HSCs and an enhanced activation of NK cells were detected. Freshly isolated HSCs from ADH3‐deficient mice showed reduced expression of collagen and TGF‐β1, but enhanced expression of IFN‐γ was detected in NK cells from these mice compared with those of control mice. Using reciprocal bone marrow transplantation of wild‐type and ADH3‐deficient mice, we demonstrated that ADH3 deficiency in both HSCs and NK cells contributed to the suppressed liver fibrosis. Conclusion: ADH3 plays important roles in promoting liver fibrosis by enhancing HSC activation and inhibiting NK cell activity, and could be used as a potential therapeutic target for the treatment of liver fibrosis. (Hepatology 2014;60:1044–1053)
doi_str_mv 10.1002/hep.27137
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Nevertheless, the expression and role of retinol metabolizing enzyme in both cell types have yet to be clarified. Thus, we investigated the expression of retinol metabolizing enzyme and its role in liver fibrosis. Among several retinol metabolizing enzymes, only alcohol dehydrogenase (ADH) 3 expression was detected in isolated HSCs and NK cells, whereas hepatocytes express all of them. In vitro treatment with 4‐methylpyrazole (4‐MP), a broad ADH inhibitor, or depletion of the ADH3 gene down‐regulated collagen and transforming growth factor‐β1 (TGF‐β1) gene expression, but did not affect α‐smooth muscle actin gene expression in cultured HSCs. Additionally, in vitro, treatments with retinol suppressed NK cell activities, whereas inhibition of ADH3 enhanced interferon‐γ (IFN‐γ) production and cytotoxicity of NK cells against HSCs. In vivo, genetic depletion of the ADH3 gene ameliorated bile duct ligation‐ and carbon tetrachloride‐induced liver fibrosis, in which a higher number of apoptotic HSCs and an enhanced activation of NK cells were detected. Freshly isolated HSCs from ADH3‐deficient mice showed reduced expression of collagen and TGF‐β1, but enhanced expression of IFN‐γ was detected in NK cells from these mice compared with those of control mice. Using reciprocal bone marrow transplantation of wild‐type and ADH3‐deficient mice, we demonstrated that ADH3 deficiency in both HSCs and NK cells contributed to the suppressed liver fibrosis. Conclusion: ADH3 plays important roles in promoting liver fibrosis by enhancing HSC activation and inhibiting NK cell activity, and could be used as a potential therapeutic target for the treatment of liver fibrosis. 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In vivo, genetic depletion of the ADH3 gene ameliorated bile duct ligation‐ and carbon tetrachloride‐induced liver fibrosis, in which a higher number of apoptotic HSCs and an enhanced activation of NK cells were detected. Freshly isolated HSCs from ADH3‐deficient mice showed reduced expression of collagen and TGF‐β1, but enhanced expression of IFN‐γ was detected in NK cells from these mice compared with those of control mice. Using reciprocal bone marrow transplantation of wild‐type and ADH3‐deficient mice, we demonstrated that ADH3 deficiency in both HSCs and NK cells contributed to the suppressed liver fibrosis. Conclusion: ADH3 plays important roles in promoting liver fibrosis by enhancing HSC activation and inhibiting NK cell activity, and could be used as a potential therapeutic target for the treatment of liver fibrosis. 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Medical Technology Development Program of the National Research Foundation funded by the Korean government (2012M3A9C7050093), the Intelligent Synthetic Biology Center of Global Frontier Project funded by the Ministry of Science, ICT &amp; Future Planning (2011‐0031955), grants of the Korean Health Technology R&amp;D Project, Ministry of Health &amp; Welfare, Republic of Korea (A111345 and A111498) and a grant from the Next‐Generation BioGreen 21 Program (No. PJ009957), Rural Development Administration, Republic of Korea</notes><notes>Potential conflict of interest: Nothing to report.</notes><notes>ObjectType-Article-1</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-2</notes><notes>content type line 23</notes><notes>Hyon-Seung Yi, jmpbooks@kaist.ac.kr; Young-Sun Lee, lys810@kaist.ac,kr; Jin-Seok Byun, jsbyun@knu.ac.kr; Wonhyo Seo, wonhyoseo@kaist.ac.kr; Jong-Min Jeong, jjmin@kaist.ac.kr; Ogyi Park, parkogyi@mail.nih.gov; Gregg Duester, duester@sanfordburnham.org; Takeshi Haseba, hasebat@nms.ac.jp; Sun Chang Kim, sunkim@kaist.ac.kr; Keun-Gyu Park, kpark@knu.ac.kr; Bin Gao, bgao@mail.nih.gov</notes><abstract>The important roles of retinols and their metabolites have recently been emphasized in the interactions between hepatic stellate cells (HSCs) and natural killer (NK) cells. Nevertheless, the expression and role of retinol metabolizing enzyme in both cell types have yet to be clarified. Thus, we investigated the expression of retinol metabolizing enzyme and its role in liver fibrosis. Among several retinol metabolizing enzymes, only alcohol dehydrogenase (ADH) 3 expression was detected in isolated HSCs and NK cells, whereas hepatocytes express all of them. In vitro treatment with 4‐methylpyrazole (4‐MP), a broad ADH inhibitor, or depletion of the ADH3 gene down‐regulated collagen and transforming growth factor‐β1 (TGF‐β1) gene expression, but did not affect α‐smooth muscle actin gene expression in cultured HSCs. Additionally, in vitro, treatments with retinol suppressed NK cell activities, whereas inhibition of ADH3 enhanced interferon‐γ (IFN‐γ) production and cytotoxicity of NK cells against HSCs. In vivo, genetic depletion of the ADH3 gene ameliorated bile duct ligation‐ and carbon tetrachloride‐induced liver fibrosis, in which a higher number of apoptotic HSCs and an enhanced activation of NK cells were detected. Freshly isolated HSCs from ADH3‐deficient mice showed reduced expression of collagen and TGF‐β1, but enhanced expression of IFN‐γ was detected in NK cells from these mice compared with those of control mice. Using reciprocal bone marrow transplantation of wild‐type and ADH3‐deficient mice, we demonstrated that ADH3 deficiency in both HSCs and NK cells contributed to the suppressed liver fibrosis. Conclusion: ADH3 plays important roles in promoting liver fibrosis by enhancing HSC activation and inhibiting NK cell activity, and could be used as a potential therapeutic target for the treatment of liver fibrosis. (Hepatology 2014;60:1044–1053)</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>24668648</pmid><doi>10.1002/hep.27137</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record>
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source Wiley-Blackwell Journals
subjects Alcohol
Aldehyde Oxidoreductases - metabolism
Animals
Bone Marrow Transplantation
Dehydrogenases
Enzymes
Gene expression
Hepatic Stellate Cells - physiology
Hepatology
Immune system
Interferon-gamma - metabolism
Killer Cells, Natural - physiology
Liver cirrhosis
Liver Cirrhosis - enzymology
Liver Cirrhosis - immunology
Male
Mice
Mice, Inbred C57BL
Rodents
title Alcohol dehydrogenase III exacerbates liver fibrosis by enhancing stellate cell activation and suppressing natural killer cells in mice
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