Analysis of the therapeutic potential of miR-124 and miR-16 in non-alcoholic fatty liver disease
Non-alcoholic fatty liver disease (NAFLD) is a common condition affecting >25 % of the population worldwide. This disorder ranges in severity from simple steatosis (fat accumulation) to severe steatohepatitis (inflammation), fibrosis and, at its end-stage, liver cancer. A number of studies have i...
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| Veröffentlicht in: | Journal of diabetes and its complications 2024-04, Vol.38 (4), p.108722-108722, Article 108722 |
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| creator | Mahmoudi, Ali Jalili, Amin Aghaee-Bakhtiari, Seyed Hamid Oskuee, Reza Kazemi Butler, Alexandra E. Rizzo, Manfredi Sahebkar, Amirhossein |
| description | Non-alcoholic fatty liver disease (NAFLD) is a common condition affecting >25 % of the population worldwide. This disorder ranges in severity from simple steatosis (fat accumulation) to severe steatohepatitis (inflammation), fibrosis and, at its end-stage, liver cancer. A number of studies have identified overexpression of several key genes that are critical in the initiation and progression of NAFLD. MiRNAs are potential therapeutic agents that can regulate several genes simultaneously. Therefore, we transfected cell lines with two key miRNAs involved in targeting NAFLD-related genes.
The suppression effects of the investigated miRNAs (miR-124 and miR-16) and genes (TNF, TLR4, SCD, FASN, SREBF2, and TGFβ-1) from our previous study were investigated by real-time PCR in Huh7 and HepG2 cells treated with oleic acid. Oil red O staining and the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assay were utilized to assess cell lipid accumulation and cytotoxic effects of the miRNAs, respectively. The pro-oxidant-antioxidant balance (PAB) assay was undertaken for miR-16 and miR-124 after cell transfection.
Following transfection of miRNAs into HepG2, oil red O staining showed miR-124 and miR-16 reduced oleic acid-induced lipid accumulation by 35.2 % and 28.6 % respectively (p |
| doi_str_mv | 10.1016/j.jdiacomp.2024.108722 |
| format | Article |
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The suppression effects of the investigated miRNAs (miR-124 and miR-16) and genes (TNF, TLR4, SCD, FASN, SREBF2, and TGFβ-1) from our previous study were investigated by real-time PCR in Huh7 and HepG2 cells treated with oleic acid. Oil red O staining and the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assay were utilized to assess cell lipid accumulation and cytotoxic effects of the miRNAs, respectively. The pro-oxidant-antioxidant balance (PAB) assay was undertaken for miR-16 and miR-124 after cell transfection.
Following transfection of miRNAs into HepG2, oil red O staining showed miR-124 and miR-16 reduced oleic acid-induced lipid accumulation by 35.2 % and 28.6 % respectively (p < 0.05). In Huh7, miR-124 and miR-16 reduced accumulation by 23.5 % and 31.3 % respectively (p < 0.05) but without impacting anti-oxidant activity. Real-time PCR in HepG2 revealed miR-124 decreased expression of TNF by 0.13-fold, TLR4 by 0.12-fold and SREBF2 by 0.127-fold (p < 0.05). miR-16 decreased TLR4 by 0.66-fold and FASN by 0.3-fold (p < 0.05). In Huh7, miR-124 decreased TNF by 0.12-fold and FASN by 0.09-fold (p < 0.05). miR-16 decreased SCD by 0.28-fold and FASN by 0.64-fold (p < 0.05). MTT assays showed, in HepG2, viability was decreased 24.7 % by miR-124 and decreased 33 % by miR-16 at 72 h (p < 0.05). In Huh7, miR-124 decreased viability 42 % at 48 h and 29.33 % at 72 h (p < 0.05), while miR-16 decreased viability by 32.3 % (p < 0.05).
These results demonstrate the ability of miR-124 and miR-16 to significantly reduce lipid accumulation and expression of key pathogenic genes associated with NAFLD through direct targeting. Though this requires further in vivo investigation.
•MiRNAs are potential therapeutic agents that can regulate several NAFLD-related genes.•We transfected cell lines with two key miRNAs involved in targeting NAFLD-related genes.•The effects of the investigated miRNAs were investigated by RT-PCR in Huh7 and HepG2 cells treated with oleic acid.•The pro-oxidant-antioxidant balance assay was undertaken for miR-16 and miR-124 after cell transfection.•miR-16 and miR-124 may have therapeutic efficacy in the treatment of NAFLD, though this requires further in vivo investigation.]]></description><identifier>ISSN: 1056-8727</identifier><identifier>EISSN: 1873-460X</identifier><identifier>DOI: 10.1016/j.jdiacomp.2024.108722</identifier><identifier>PMID: 38503000</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Bioinformatics ; Cancer therapies ; Cytokines ; Genes ; Genomes ; Inflammation ; Lipids ; Liver cancer ; Liver diseases ; Metabolism ; MicroRNAs ; Microscopy ; miR-124 ; miR-16 ; NAFLD ; Oxidative stress ; Plasmids ; Real-time PCR ; Transfection ; Tumor necrosis factor-TNF ; Tumors</subject><ispartof>Journal of diabetes and its complications, 2024-04, Vol.38 (4), p.108722-108722, Article 108722</ispartof><rights>2024 Elsevier Inc.</rights><rights>Copyright © 2024 Elsevier Inc. All rights reserved.</rights><rights>2024. Elsevier Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c396t-7920c7889632bc843ecd2e0c5f7da88ec670d107c3ce275ef5f7817c88faa0473</citedby><cites>FETCH-LOGICAL-c396t-7920c7889632bc843ecd2e0c5f7da88ec670d107c3ce275ef5f7817c88faa0473</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.proquest.com/docview/2985830497?pq-origsite=primo$$EHTML$$P50$$Gproquest$$H</linktohtml><link.rule.ids>314,778,782,3539,27907,27908,45978,64366,64368,64370,72220</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38503000$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mahmoudi, Ali</creatorcontrib><creatorcontrib>Jalili, Amin</creatorcontrib><creatorcontrib>Aghaee-Bakhtiari, Seyed Hamid</creatorcontrib><creatorcontrib>Oskuee, Reza Kazemi</creatorcontrib><creatorcontrib>Butler, Alexandra E.</creatorcontrib><creatorcontrib>Rizzo, Manfredi</creatorcontrib><creatorcontrib>Sahebkar, Amirhossein</creatorcontrib><title>Analysis of the therapeutic potential of miR-124 and miR-16 in non-alcoholic fatty liver disease</title><title>Journal of diabetes and its complications</title><addtitle>J Diabetes Complications</addtitle><description><![CDATA[Non-alcoholic fatty liver disease (NAFLD) is a common condition affecting >25 % of the population worldwide. This disorder ranges in severity from simple steatosis (fat accumulation) to severe steatohepatitis (inflammation), fibrosis and, at its end-stage, liver cancer. A number of studies have identified overexpression of several key genes that are critical in the initiation and progression of NAFLD. MiRNAs are potential therapeutic agents that can regulate several genes simultaneously. Therefore, we transfected cell lines with two key miRNAs involved in targeting NAFLD-related genes.
The suppression effects of the investigated miRNAs (miR-124 and miR-16) and genes (TNF, TLR4, SCD, FASN, SREBF2, and TGFβ-1) from our previous study were investigated by real-time PCR in Huh7 and HepG2 cells treated with oleic acid. Oil red O staining and the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assay were utilized to assess cell lipid accumulation and cytotoxic effects of the miRNAs, respectively. The pro-oxidant-antioxidant balance (PAB) assay was undertaken for miR-16 and miR-124 after cell transfection.
Following transfection of miRNAs into HepG2, oil red O staining showed miR-124 and miR-16 reduced oleic acid-induced lipid accumulation by 35.2 % and 28.6 % respectively (p < 0.05). In Huh7, miR-124 and miR-16 reduced accumulation by 23.5 % and 31.3 % respectively (p < 0.05) but without impacting anti-oxidant activity. Real-time PCR in HepG2 revealed miR-124 decreased expression of TNF by 0.13-fold, TLR4 by 0.12-fold and SREBF2 by 0.127-fold (p < 0.05). miR-16 decreased TLR4 by 0.66-fold and FASN by 0.3-fold (p < 0.05). In Huh7, miR-124 decreased TNF by 0.12-fold and FASN by 0.09-fold (p < 0.05). miR-16 decreased SCD by 0.28-fold and FASN by 0.64-fold (p < 0.05). MTT assays showed, in HepG2, viability was decreased 24.7 % by miR-124 and decreased 33 % by miR-16 at 72 h (p < 0.05). In Huh7, miR-124 decreased viability 42 % at 48 h and 29.33 % at 72 h (p < 0.05), while miR-16 decreased viability by 32.3 % (p < 0.05).
These results demonstrate the ability of miR-124 and miR-16 to significantly reduce lipid accumulation and expression of key pathogenic genes associated with NAFLD through direct targeting. Though this requires further in vivo investigation.
•MiRNAs are potential therapeutic agents that can regulate several NAFLD-related genes.•We transfected cell lines with two key miRNAs involved in targeting NAFLD-related genes.•The effects of the investigated miRNAs were investigated by RT-PCR in Huh7 and HepG2 cells treated with oleic acid.•The pro-oxidant-antioxidant balance assay was undertaken for miR-16 and miR-124 after cell transfection.•miR-16 and miR-124 may have therapeutic efficacy in the treatment of NAFLD, though this requires further in vivo investigation.]]></description><subject>Bioinformatics</subject><subject>Cancer therapies</subject><subject>Cytokines</subject><subject>Genes</subject><subject>Genomes</subject><subject>Inflammation</subject><subject>Lipids</subject><subject>Liver cancer</subject><subject>Liver diseases</subject><subject>Metabolism</subject><subject>MicroRNAs</subject><subject>Microscopy</subject><subject>miR-124</subject><subject>miR-16</subject><subject>NAFLD</subject><subject>Oxidative stress</subject><subject>Plasmids</subject><subject>Real-time PCR</subject><subject>Transfection</subject><subject>Tumor necrosis factor-TNF</subject><subject>Tumors</subject><issn>1056-8727</issn><issn>1873-460X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqFkctq3jAQhUVpadK0rxAM3XTjv7rYkrxrCOkFAoHQQHaqMhoTGdtyJTnwv31lnHTRTRdCo5nvjOAcQs4ZPTDK5OfhMDhvIUzLgVPelKZWnL8ip0wrUTeS3r8uNW1lXfrqhLxLaaCUyrZlb8mJ0C0V5XlKfl3Mdjwmn6rQV_kRtxPtgmv2UC0h45y9Hbfh5G9rxpvKzm6vZeXnag5zbUcIj2Esgt7mfKxG_4Sxcj6hTfievOntmPDD831G7r5e_bz8Xl_ffPtxeXFdg-hkrlXHKSitOyn4A-hGIDiOFNpeOas1glTUMapAAHLVYl8GminQureWNkqckU_73iWG3yumbCafAMfRzhjWZHhXfKBCclbQj_-gQ1hj8WGjdKsFbbptodwpiCGliL1Zop9sPBpGzZaBGcxLBmbLwOwZFOH58_r1YUL3V_ZiegG-7AAWP548RpPA4wzofETIxgX_vz_-AN02mYg</recordid><startdate>20240401</startdate><enddate>20240401</enddate><creator>Mahmoudi, Ali</creator><creator>Jalili, Amin</creator><creator>Aghaee-Bakhtiari, Seyed Hamid</creator><creator>Oskuee, Reza Kazemi</creator><creator>Butler, Alexandra E.</creator><creator>Rizzo, Manfredi</creator><creator>Sahebkar, Amirhossein</creator><general>Elsevier Inc</general><general>Elsevier Limited</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>ASE</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FPQ</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K6X</scope><scope>K9-</scope><scope>K9.</scope><scope>KB0</scope><scope>M0R</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>20240401</creationdate><title>Analysis of the therapeutic potential of miR-124 and miR-16 in non-alcoholic fatty liver disease</title><author>Mahmoudi, Ali ; Jalili, Amin ; Aghaee-Bakhtiari, Seyed Hamid ; Oskuee, Reza Kazemi ; Butler, Alexandra E. ; Rizzo, Manfredi ; Sahebkar, Amirhossein</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c396t-7920c7889632bc843ecd2e0c5f7da88ec670d107c3ce275ef5f7817c88faa0473</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Bioinformatics</topic><topic>Cancer therapies</topic><topic>Cytokines</topic><topic>Genes</topic><topic>Genomes</topic><topic>Inflammation</topic><topic>Lipids</topic><topic>Liver cancer</topic><topic>Liver diseases</topic><topic>Metabolism</topic><topic>MicroRNAs</topic><topic>Microscopy</topic><topic>miR-124</topic><topic>miR-16</topic><topic>NAFLD</topic><topic>Oxidative stress</topic><topic>Plasmids</topic><topic>Real-time PCR</topic><topic>Transfection</topic><topic>Tumor necrosis factor-TNF</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Mahmoudi, Ali</creatorcontrib><creatorcontrib>Jalili, Amin</creatorcontrib><creatorcontrib>Aghaee-Bakhtiari, Seyed Hamid</creatorcontrib><creatorcontrib>Oskuee, Reza Kazemi</creatorcontrib><creatorcontrib>Butler, Alexandra E.</creatorcontrib><creatorcontrib>Rizzo, Manfredi</creatorcontrib><creatorcontrib>Sahebkar, Amirhossein</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</collection><collection>British Nursing Index</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>British Nursing Index (BNI) (1985 to Present)</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>British Nursing Index</collection><collection>Consumer Health Database (Alumni Edition)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Consumer Health Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of diabetes and its complications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Mahmoudi, Ali</au><au>Jalili, Amin</au><au>Aghaee-Bakhtiari, Seyed Hamid</au><au>Oskuee, Reza Kazemi</au><au>Butler, Alexandra E.</au><au>Rizzo, Manfredi</au><au>Sahebkar, Amirhossein</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Analysis of the therapeutic potential of miR-124 and miR-16 in non-alcoholic fatty liver disease</atitle><jtitle>Journal of diabetes and its complications</jtitle><addtitle>J Diabetes Complications</addtitle><date>2024-04-01</date><risdate>2024</risdate><volume>38</volume><issue>4</issue><spage>108722</spage><epage>108722</epage><pages>108722-108722</pages><artnum>108722</artnum><issn>1056-8727</issn><eissn>1873-460X</eissn><abstract><![CDATA[Non-alcoholic fatty liver disease (NAFLD) is a common condition affecting >25 % of the population worldwide. This disorder ranges in severity from simple steatosis (fat accumulation) to severe steatohepatitis (inflammation), fibrosis and, at its end-stage, liver cancer. A number of studies have identified overexpression of several key genes that are critical in the initiation and progression of NAFLD. MiRNAs are potential therapeutic agents that can regulate several genes simultaneously. Therefore, we transfected cell lines with two key miRNAs involved in targeting NAFLD-related genes.
The suppression effects of the investigated miRNAs (miR-124 and miR-16) and genes (TNF, TLR4, SCD, FASN, SREBF2, and TGFβ-1) from our previous study were investigated by real-time PCR in Huh7 and HepG2 cells treated with oleic acid. Oil red O staining and the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assay were utilized to assess cell lipid accumulation and cytotoxic effects of the miRNAs, respectively. The pro-oxidant-antioxidant balance (PAB) assay was undertaken for miR-16 and miR-124 after cell transfection.
Following transfection of miRNAs into HepG2, oil red O staining showed miR-124 and miR-16 reduced oleic acid-induced lipid accumulation by 35.2 % and 28.6 % respectively (p < 0.05). In Huh7, miR-124 and miR-16 reduced accumulation by 23.5 % and 31.3 % respectively (p < 0.05) but without impacting anti-oxidant activity. Real-time PCR in HepG2 revealed miR-124 decreased expression of TNF by 0.13-fold, TLR4 by 0.12-fold and SREBF2 by 0.127-fold (p < 0.05). miR-16 decreased TLR4 by 0.66-fold and FASN by 0.3-fold (p < 0.05). In Huh7, miR-124 decreased TNF by 0.12-fold and FASN by 0.09-fold (p < 0.05). miR-16 decreased SCD by 0.28-fold and FASN by 0.64-fold (p < 0.05). MTT assays showed, in HepG2, viability was decreased 24.7 % by miR-124 and decreased 33 % by miR-16 at 72 h (p < 0.05). In Huh7, miR-124 decreased viability 42 % at 48 h and 29.33 % at 72 h (p < 0.05), while miR-16 decreased viability by 32.3 % (p < 0.05).
These results demonstrate the ability of miR-124 and miR-16 to significantly reduce lipid accumulation and expression of key pathogenic genes associated with NAFLD through direct targeting. Though this requires further in vivo investigation.
•MiRNAs are potential therapeutic agents that can regulate several NAFLD-related genes.•We transfected cell lines with two key miRNAs involved in targeting NAFLD-related genes.•The effects of the investigated miRNAs were investigated by RT-PCR in Huh7 and HepG2 cells treated with oleic acid.•The pro-oxidant-antioxidant balance assay was undertaken for miR-16 and miR-124 after cell transfection.•miR-16 and miR-124 may have therapeutic efficacy in the treatment of NAFLD, though this requires further in vivo investigation.]]></abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>38503000</pmid><doi>10.1016/j.jdiacomp.2024.108722</doi><tpages>1</tpages></addata></record> |
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| ispartof | Journal of diabetes and its complications, 2024-04, Vol.38 (4), p.108722-108722, Article 108722 |
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| source | ScienceDirect Journals (5 years ago - present); ProQuest Central UK/Ireland |
| subjects | Bioinformatics Cancer therapies Cytokines Genes Genomes Inflammation Lipids Liver cancer Liver diseases Metabolism MicroRNAs Microscopy miR-124 miR-16 NAFLD Oxidative stress Plasmids Real-time PCR Transfection Tumor necrosis factor-TNF Tumors |
| title | Analysis of the therapeutic potential of miR-124 and miR-16 in non-alcoholic fatty liver disease |
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