The Role of Zinc on Liver Fibrosis by Modulating ZIP14 Expression Throughout Epigenetic Regulatory Mechanisms
Zinc plays a pivotal role in tissue regeneration and maintenance being as a central cofactor in a plethora of enzymatic activities. Hypozincemia is commonly seen with chronic liver disease and is associated with an increased risk of liver fibrosis development and hepatocellular carcinoma. Previously...
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| Veröffentlicht in: | Biological trace element research 2024-11, Vol.202 (11), p.5094-5105 |
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| creator | Aksoy-Ozer, Zeynep Busra Bitirim, Ceylan Verda Turan, Belma Akcali, Kamil Can |
| description | Zinc plays a pivotal role in tissue regeneration and maintenance being as a central cofactor in a plethora of enzymatic activities. Hypozincemia is commonly seen with chronic liver disease and is associated with an increased risk of liver fibrosis development and hepatocellular carcinoma. Previously favorable effects of zinc supplementation on liver fibrosis have been shown. However, the underlying mechanism of this effect is not elucidated. Liver fibrosis was induced in mice by using CCl
4
injection, followed by treatment with zinc chloride (ZnCl
2
) both at fibrotic and sham groups, and their hepatocytes were isolated. Our results showed that the administration of ZnCl
2
restored the depleted cytosolic zinc levels in the hepatocytes isolated from the fibrotic group. Also, alpha-smooth muscle actin (
αSMA
) expression in hepatocytes was decreased, indicating a reversal of the fibrotic process. Notably, ZIP14 expression significantly increased in the fibrotic group following ZnCl
2
treatment, whereas in the sham group ZIP14 expression decreased. Chromatin immunoprecipitation (ChIP) experiments revealed an increased binding percentage of Metal-regulatory transcription factor 1 (MTF1) on
ZIP14
promoter in the hepatocytes isolated from fibrotic mice compared to the sham group after ZnCl
2
administration. In the same group, the binding percentage of the histone deacetylase HDAC4 on
ZIP14
promoter decreased. Our results suggest that the ZnCl
2
treatment ameliorates liver fibrosis by elevating intracellular zinc levels through MTF1-mediated regulation of
ZIP14
expression and the reduction of
ZIP14
deacetylation via HDAC4. The restoration of intracellular zinc concentrations and the modulation of
ZIP14
expression by zinc orchestrated through MTF1 and HDAC4, appear to be essential determinants of the therapeutic response in hepatic fibrosis. These findings pave the way for potential novel interventions targeting zinc-related pathways for the treatment of liver fibrosis and associated conditions. |
| doi_str_mv | 10.1007/s12011-023-04057-5 |
| format | Article |
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4
injection, followed by treatment with zinc chloride (ZnCl
2
) both at fibrotic and sham groups, and their hepatocytes were isolated. Our results showed that the administration of ZnCl
2
restored the depleted cytosolic zinc levels in the hepatocytes isolated from the fibrotic group. Also, alpha-smooth muscle actin (
αSMA
) expression in hepatocytes was decreased, indicating a reversal of the fibrotic process. Notably, ZIP14 expression significantly increased in the fibrotic group following ZnCl
2
treatment, whereas in the sham group ZIP14 expression decreased. Chromatin immunoprecipitation (ChIP) experiments revealed an increased binding percentage of Metal-regulatory transcription factor 1 (MTF1) on
ZIP14
promoter in the hepatocytes isolated from fibrotic mice compared to the sham group after ZnCl
2
administration. In the same group, the binding percentage of the histone deacetylase HDAC4 on
ZIP14
promoter decreased. Our results suggest that the ZnCl
2
treatment ameliorates liver fibrosis by elevating intracellular zinc levels through MTF1-mediated regulation of
ZIP14
expression and the reduction of
ZIP14
deacetylation via HDAC4. The restoration of intracellular zinc concentrations and the modulation of
ZIP14
expression by zinc orchestrated through MTF1 and HDAC4, appear to be essential determinants of the therapeutic response in hepatic fibrosis. These findings pave the way for potential novel interventions targeting zinc-related pathways for the treatment of liver fibrosis and associated conditions.</description><identifier>ISSN: 0163-4984</identifier><identifier>ISSN: 1559-0720</identifier><identifier>EISSN: 1559-0720</identifier><identifier>DOI: 10.1007/s12011-023-04057-5</identifier><identifier>PMID: 38221603</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Actin ; Animals ; Binding ; Biochemistry ; Biomedical and Life Sciences ; Biotechnology ; Carbon Tetrachloride ; Cation Transport Proteins - genetics ; Cation Transport Proteins - metabolism ; Chlorides - metabolism ; Chlorides - pharmacology ; Chromatin ; Deacetylation ; DNA-Binding Proteins - genetics ; DNA-Binding Proteins - metabolism ; Enzymatic activity ; Enzyme activity ; Epigenesis, Genetic - drug effects ; Epigenetics ; Fibrosis ; Heavy metals ; Hepatocellular carcinoma ; Hepatocytes ; Hepatocytes - drug effects ; Hepatocytes - metabolism ; Histone deacetylase ; Histone Deacetylases - metabolism ; Histones ; Immunoprecipitation ; Intracellular ; Life Sciences ; Liver ; Liver cirrhosis ; Liver Cirrhosis - chemically induced ; Liver Cirrhosis - drug therapy ; Liver Cirrhosis - metabolism ; Liver Cirrhosis - pathology ; Liver diseases ; Male ; Mice ; Mice, Inbred C57BL ; Neoplasms ; Nutrition ; Oncology ; Promoter Regions, Genetic ; Promoters ; Regeneration (biological) ; Regeneration (physiology) ; Regulatory mechanisms (biology) ; Smooth muscle ; Tissue engineering ; Transcription Factor MTF-1 ; Transcription Factors - genetics ; Transcription Factors - metabolism ; Zinc ; Zinc - metabolism ; Zinc - pharmacology ; Zinc chloride ; Zinc Compounds - pharmacology</subject><ispartof>Biological trace element research, 2024-11, Vol.202 (11), p.5094-5105</ispartof><rights>The Author(s) 2024</rights><rights>2024. The Author(s).</rights><rights>The Author(s) 2024. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>The Author(s) 2024 2024</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c426t-c0474b08cb5252fb8113b5861f772e585e38c2e2f44bb2ee1ff259fc1204e2b53</cites><orcidid>0000-0002-7979-0679 ; 0000-0002-8288-0974 ; 0000-0003-2583-9294 ; 0000-0002-7816-6938</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12011-023-04057-5$$EPDF$$P50$$Gspringer$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12011-023-04057-5$$EHTML$$P50$$Gspringer$$Hfree_for_read</linktohtml><link.rule.ids>230,314,780,784,885,27922,27923,41486,42555,51317</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38221603$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Aksoy-Ozer, Zeynep Busra</creatorcontrib><creatorcontrib>Bitirim, Ceylan Verda</creatorcontrib><creatorcontrib>Turan, Belma</creatorcontrib><creatorcontrib>Akcali, Kamil Can</creatorcontrib><title>The Role of Zinc on Liver Fibrosis by Modulating ZIP14 Expression Throughout Epigenetic Regulatory Mechanisms</title><title>Biological trace element research</title><addtitle>Biol Trace Elem Res</addtitle><addtitle>Biol Trace Elem Res</addtitle><description>Zinc plays a pivotal role in tissue regeneration and maintenance being as a central cofactor in a plethora of enzymatic activities. Hypozincemia is commonly seen with chronic liver disease and is associated with an increased risk of liver fibrosis development and hepatocellular carcinoma. Previously favorable effects of zinc supplementation on liver fibrosis have been shown. However, the underlying mechanism of this effect is not elucidated. Liver fibrosis was induced in mice by using CCl
4
injection, followed by treatment with zinc chloride (ZnCl
2
) both at fibrotic and sham groups, and their hepatocytes were isolated. Our results showed that the administration of ZnCl
2
restored the depleted cytosolic zinc levels in the hepatocytes isolated from the fibrotic group. Also, alpha-smooth muscle actin (
αSMA
) expression in hepatocytes was decreased, indicating a reversal of the fibrotic process. Notably, ZIP14 expression significantly increased in the fibrotic group following ZnCl
2
treatment, whereas in the sham group ZIP14 expression decreased. Chromatin immunoprecipitation (ChIP) experiments revealed an increased binding percentage of Metal-regulatory transcription factor 1 (MTF1) on
ZIP14
promoter in the hepatocytes isolated from fibrotic mice compared to the sham group after ZnCl
2
administration. In the same group, the binding percentage of the histone deacetylase HDAC4 on
ZIP14
promoter decreased. Our results suggest that the ZnCl
2
treatment ameliorates liver fibrosis by elevating intracellular zinc levels through MTF1-mediated regulation of
ZIP14
expression and the reduction of
ZIP14
deacetylation via HDAC4. The restoration of intracellular zinc concentrations and the modulation of
ZIP14
expression by zinc orchestrated through MTF1 and HDAC4, appear to be essential determinants of the therapeutic response in hepatic fibrosis. These findings pave the way for potential novel interventions targeting zinc-related pathways for the treatment of liver fibrosis and associated conditions.</description><subject>Actin</subject><subject>Animals</subject><subject>Binding</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Biotechnology</subject><subject>Carbon Tetrachloride</subject><subject>Cation Transport Proteins - genetics</subject><subject>Cation Transport Proteins - metabolism</subject><subject>Chlorides - metabolism</subject><subject>Chlorides - pharmacology</subject><subject>Chromatin</subject><subject>Deacetylation</subject><subject>DNA-Binding Proteins - genetics</subject><subject>DNA-Binding Proteins - metabolism</subject><subject>Enzymatic activity</subject><subject>Enzyme activity</subject><subject>Epigenesis, Genetic - drug effects</subject><subject>Epigenetics</subject><subject>Fibrosis</subject><subject>Heavy metals</subject><subject>Hepatocellular carcinoma</subject><subject>Hepatocytes</subject><subject>Hepatocytes - drug effects</subject><subject>Hepatocytes - metabolism</subject><subject>Histone deacetylase</subject><subject>Histone Deacetylases - metabolism</subject><subject>Histones</subject><subject>Immunoprecipitation</subject><subject>Intracellular</subject><subject>Life Sciences</subject><subject>Liver</subject><subject>Liver cirrhosis</subject><subject>Liver Cirrhosis - chemically induced</subject><subject>Liver Cirrhosis - drug therapy</subject><subject>Liver Cirrhosis - metabolism</subject><subject>Liver Cirrhosis - pathology</subject><subject>Liver diseases</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Neoplasms</subject><subject>Nutrition</subject><subject>Oncology</subject><subject>Promoter Regions, Genetic</subject><subject>Promoters</subject><subject>Regeneration (biological)</subject><subject>Regeneration (physiology)</subject><subject>Regulatory mechanisms (biology)</subject><subject>Smooth muscle</subject><subject>Tissue engineering</subject><subject>Transcription Factor MTF-1</subject><subject>Transcription Factors - genetics</subject><subject>Transcription Factors - metabolism</subject><subject>Zinc</subject><subject>Zinc - metabolism</subject><subject>Zinc - pharmacology</subject><subject>Zinc chloride</subject><subject>Zinc Compounds - pharmacology</subject><issn>0163-4984</issn><issn>1559-0720</issn><issn>1559-0720</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><recordid>eNp9kUtv1DAUhS0EotPCH2CBLLHpJuDrRx4rhKppqTQIVA2bbqzYvUlcJfZgJxX993iYUh4LVl7cc47vuR8hr4C9Bcaqdwk4AygYFwWTTFWFekJWoFRTsIqzp2TFoBSFbGp5RI5TumUMKt6I5-RI1JxDycSKTNsB6VUYkYaOXjtvafB04-4w0nNnYkguUXNPP4WbZWxn53t6ffkFJF1_30VMyWX1dohh6YewzHS9cz16nJ2lV9jvHSFmM9qh9S5N6QV51rVjwpcP7wn5er7enn0sNp8vLs8-bAoreTkXlslKGlZbo7jinakBhFF1CV1VcVS1QlFbjryT0hiOCF3HVdPZfA-J3ChxQt4fcneLmfDGop9jO-pddFMb73Vonf574t2g-3CnAaTksqpywulDQgzfFkyznlyyOI6tx7AkzRuQXJU11Fn65h_pbViiz_20gLx5mSHtA_lBZfNRU8TucRtgeo9TH3DqjFP_xKn3PV7_2ePR8otfFoiDIOWR7zH-_vs_sT8AxS-rLA</recordid><startdate>202411</startdate><enddate>202411</enddate><creator>Aksoy-Ozer, Zeynep Busra</creator><creator>Bitirim, Ceylan Verda</creator><creator>Turan, Belma</creator><creator>Akcali, Kamil Can</creator><general>Springer US</general><general>Springer Nature B.V</general><scope>C6C</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QH</scope><scope>7QP</scope><scope>7TN</scope><scope>7U7</scope><scope>7UA</scope><scope>C1K</scope><scope>F1W</scope><scope>H97</scope><scope>K9.</scope><scope>L.G</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-7979-0679</orcidid><orcidid>https://orcid.org/0000-0002-8288-0974</orcidid><orcidid>https://orcid.org/0000-0003-2583-9294</orcidid><orcidid>https://orcid.org/0000-0002-7816-6938</orcidid></search><sort><creationdate>202411</creationdate><title>The Role of Zinc on Liver Fibrosis by Modulating ZIP14 Expression Throughout Epigenetic Regulatory Mechanisms</title><author>Aksoy-Ozer, Zeynep Busra ; Bitirim, Ceylan Verda ; Turan, Belma ; Akcali, Kamil Can</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c426t-c0474b08cb5252fb8113b5861f772e585e38c2e2f44bb2ee1ff259fc1204e2b53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Actin</topic><topic>Animals</topic><topic>Binding</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Biotechnology</topic><topic>Carbon Tetrachloride</topic><topic>Cation Transport Proteins - genetics</topic><topic>Cation Transport Proteins - metabolism</topic><topic>Chlorides - metabolism</topic><topic>Chlorides - pharmacology</topic><topic>Chromatin</topic><topic>Deacetylation</topic><topic>DNA-Binding Proteins - genetics</topic><topic>DNA-Binding Proteins - metabolism</topic><topic>Enzymatic activity</topic><topic>Enzyme activity</topic><topic>Epigenesis, Genetic - drug effects</topic><topic>Epigenetics</topic><topic>Fibrosis</topic><topic>Heavy metals</topic><topic>Hepatocellular carcinoma</topic><topic>Hepatocytes</topic><topic>Hepatocytes - drug effects</topic><topic>Hepatocytes - metabolism</topic><topic>Histone deacetylase</topic><topic>Histone Deacetylases - metabolism</topic><topic>Histones</topic><topic>Immunoprecipitation</topic><topic>Intracellular</topic><topic>Life Sciences</topic><topic>Liver</topic><topic>Liver cirrhosis</topic><topic>Liver Cirrhosis - chemically induced</topic><topic>Liver Cirrhosis - drug therapy</topic><topic>Liver Cirrhosis - metabolism</topic><topic>Liver Cirrhosis - pathology</topic><topic>Liver diseases</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Neoplasms</topic><topic>Nutrition</topic><topic>Oncology</topic><topic>Promoter Regions, Genetic</topic><topic>Promoters</topic><topic>Regeneration (biological)</topic><topic>Regeneration (physiology)</topic><topic>Regulatory mechanisms (biology)</topic><topic>Smooth muscle</topic><topic>Tissue engineering</topic><topic>Transcription Factor MTF-1</topic><topic>Transcription Factors - genetics</topic><topic>Transcription Factors - metabolism</topic><topic>Zinc</topic><topic>Zinc - metabolism</topic><topic>Zinc - pharmacology</topic><topic>Zinc chloride</topic><topic>Zinc Compounds - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Aksoy-Ozer, Zeynep Busra</creatorcontrib><creatorcontrib>Bitirim, Ceylan Verda</creatorcontrib><creatorcontrib>Turan, Belma</creatorcontrib><creatorcontrib>Akcali, Kamil Can</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Aqualine</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Oceanic Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Water Resources Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ASFA: Aquatic Sciences and Fisheries Abstracts</collection><collection>Aquatic Science & Fisheries Abstracts (ASFA) 3: Aquatic Pollution & Environmental Quality</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Aquatic Science & Fisheries Abstracts (ASFA) Professional</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Biological trace element research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Aksoy-Ozer, Zeynep Busra</au><au>Bitirim, Ceylan Verda</au><au>Turan, Belma</au><au>Akcali, Kamil Can</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Role of Zinc on Liver Fibrosis by Modulating ZIP14 Expression Throughout Epigenetic Regulatory Mechanisms</atitle><jtitle>Biological trace element research</jtitle><stitle>Biol Trace Elem Res</stitle><addtitle>Biol Trace Elem Res</addtitle><date>2024-11</date><risdate>2024</risdate><volume>202</volume><issue>11</issue><spage>5094</spage><epage>5105</epage><pages>5094-5105</pages><issn>0163-4984</issn><issn>1559-0720</issn><eissn>1559-0720</eissn><abstract>Zinc plays a pivotal role in tissue regeneration and maintenance being as a central cofactor in a plethora of enzymatic activities. Hypozincemia is commonly seen with chronic liver disease and is associated with an increased risk of liver fibrosis development and hepatocellular carcinoma. Previously favorable effects of zinc supplementation on liver fibrosis have been shown. However, the underlying mechanism of this effect is not elucidated. Liver fibrosis was induced in mice by using CCl
4
injection, followed by treatment with zinc chloride (ZnCl
2
) both at fibrotic and sham groups, and their hepatocytes were isolated. Our results showed that the administration of ZnCl
2
restored the depleted cytosolic zinc levels in the hepatocytes isolated from the fibrotic group. Also, alpha-smooth muscle actin (
αSMA
) expression in hepatocytes was decreased, indicating a reversal of the fibrotic process. Notably, ZIP14 expression significantly increased in the fibrotic group following ZnCl
2
treatment, whereas in the sham group ZIP14 expression decreased. Chromatin immunoprecipitation (ChIP) experiments revealed an increased binding percentage of Metal-regulatory transcription factor 1 (MTF1) on
ZIP14
promoter in the hepatocytes isolated from fibrotic mice compared to the sham group after ZnCl
2
administration. In the same group, the binding percentage of the histone deacetylase HDAC4 on
ZIP14
promoter decreased. Our results suggest that the ZnCl
2
treatment ameliorates liver fibrosis by elevating intracellular zinc levels through MTF1-mediated regulation of
ZIP14
expression and the reduction of
ZIP14
deacetylation via HDAC4. The restoration of intracellular zinc concentrations and the modulation of
ZIP14
expression by zinc orchestrated through MTF1 and HDAC4, appear to be essential determinants of the therapeutic response in hepatic fibrosis. These findings pave the way for potential novel interventions targeting zinc-related pathways for the treatment of liver fibrosis and associated conditions.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>38221603</pmid><doi>10.1007/s12011-023-04057-5</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0002-7979-0679</orcidid><orcidid>https://orcid.org/0000-0002-8288-0974</orcidid><orcidid>https://orcid.org/0000-0003-2583-9294</orcidid><orcidid>https://orcid.org/0000-0002-7816-6938</orcidid><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; SpringerLink Journals - AutoHoldings |
| subjects | Actin Animals Binding Biochemistry Biomedical and Life Sciences Biotechnology Carbon Tetrachloride Cation Transport Proteins - genetics Cation Transport Proteins - metabolism Chlorides - metabolism Chlorides - pharmacology Chromatin Deacetylation DNA-Binding Proteins - genetics DNA-Binding Proteins - metabolism Enzymatic activity Enzyme activity Epigenesis, Genetic - drug effects Epigenetics Fibrosis Heavy metals Hepatocellular carcinoma Hepatocytes Hepatocytes - drug effects Hepatocytes - metabolism Histone deacetylase Histone Deacetylases - metabolism Histones Immunoprecipitation Intracellular Life Sciences Liver Liver cirrhosis Liver Cirrhosis - chemically induced Liver Cirrhosis - drug therapy Liver Cirrhosis - metabolism Liver Cirrhosis - pathology Liver diseases Male Mice Mice, Inbred C57BL Neoplasms Nutrition Oncology Promoter Regions, Genetic Promoters Regeneration (biological) Regeneration (physiology) Regulatory mechanisms (biology) Smooth muscle Tissue engineering Transcription Factor MTF-1 Transcription Factors - genetics Transcription Factors - metabolism Zinc Zinc - metabolism Zinc - pharmacology Zinc chloride Zinc Compounds - pharmacology |
| title | The Role of Zinc on Liver Fibrosis by Modulating ZIP14 Expression Throughout Epigenetic Regulatory Mechanisms |
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