Upregulation of MiR-122 via Trichostatin A Treatments in Hepatocyte-like Cells Derived from Mesenchymal Stem Cells
The miR‐122 is a tissue‐specific miRNA; its expression is abundant in liver. MiR‐122 upregulation is crucial for differentiation, functionality, and maintenance of differentiated phenotype in hepatocytes. The improving effects of trichostatin A (TSA) on hepatic differentiation have been reported pre...
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Veröffentlicht in: | Chemical biology & drug design 2016-02, Vol.87 (2), p.296-305 |
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description | The miR‐122 is a tissue‐specific miRNA; its expression is abundant in liver. MiR‐122 upregulation is crucial for differentiation, functionality, and maintenance of differentiated phenotype in hepatocytes. The improving effects of trichostatin A (TSA) on hepatic differentiation have been reported previously. The aim of this study was to determine whether TSA can affect the expression of miR‐122 in hepatocyte‐like cells (HLCs) generated from human adipose tissue‐derived mesenchymal stem cells (hAT‐MSCs). The hepatic differentiation of hAT‐MSCs induced by a mixture of growth factors and cytokines either with or without TSA treatments. The functionality of HLCs generated with or without TSA and the expression levels of miR‐122 were studied. The expression levels of miR‐122 in TSA‐treated HLCs was significantly (p < 0.05) higher than those generated by growth factors and cytokines, only. The downregulation of a‐fetoprotein (AFP) levels but enhanced albumin synthesis (p < 0.05) and upregulation of liver‐enriched transcription factors (LETFs) HNF4α (hepatocyte nuclear factor 4α) and HNF6 (hepatocyte nuclear factor 6) were observed in TSA‐treated HLCs (p < 0.05). In conclusion, administration of TSA in hepatogenic differentiation of hAT‐MSCs resulted in higher expression levels of miR‐122, facilitation of differentiation, and subsequently attenuation of AFP levels.
Administration of TSA during hepatic differentiation of adipose tissue derived mesenchymal stem cells (AT‐MSCs) resulted in the facilitation of hepatic differentiation, higher miR‐ 122 expression levels, and subsequently attenuation of AFP expression in hepatocyte like cells. |
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Administration of TSA during hepatic differentiation of adipose tissue derived mesenchymal stem cells (AT‐MSCs) resulted in the facilitation of hepatic differentiation, higher miR‐ 122 expression levels, and subsequently attenuation of AFP expression in hepatocyte like cells.</description><identifier>ISSN: 1747-0277</identifier><identifier>EISSN: 1747-0285</identifier><identifier>DOI: 10.1111/cbdd.12664</identifier><identifier>PMID: 26360933</identifier><language>eng</language><publisher>England: Blackwell Publishing Ltd</publisher><subject>alpha-Fetoproteins - metabolism ; Cell Differentiation - drug effects ; Cell Lineage ; Cells, Cultured ; Down-Regulation - drug effects ; Hepatocyte Nuclear Factor 4 - metabolism ; Hepatocyte Nuclear Factor 6 - metabolism ; hepatocyte-like cells ; Hepatocytes - cytology ; Hepatocytes - drug effects ; Hepatocytes - metabolism ; HNF4a ; HNF6 ; Humans ; Hydroxamic Acids - pharmacology ; mesenchymal stem cells ; Mesenchymal Stromal Cells - cytology ; MicroRNAs - metabolism ; miR-122 ; trichostatin A ; Up-Regulation - drug effects ; α-fetoprotein</subject><ispartof>Chemical biology & drug design, 2016-02, Vol.87 (2), p.296-305</ispartof><rights>2015 John Wiley & Sons A/S</rights><rights>2015 John Wiley & Sons A/S.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3674-55daab9d418ed67546e5013d0648ddd009051ab21d53df0cf7117abc38bc7b323</citedby><cites>FETCH-LOGICAL-c3674-55daab9d418ed67546e5013d0648ddd009051ab21d53df0cf7117abc38bc7b323</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fcbdd.12664$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fcbdd.12664$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27903,27904,45553,45554</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26360933$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Alizadeh, Effat</creatorcontrib><creatorcontrib>Eslaminejad, MohamadReza Baghaban</creatorcontrib><creatorcontrib>Akbarzadeh, Abolfazl</creatorcontrib><creatorcontrib>Sadeghi, Zohre</creatorcontrib><creatorcontrib>Abasi, Mozghan</creatorcontrib><creatorcontrib>Herizchi, Roya</creatorcontrib><creatorcontrib>Zarghami, Nosratollah</creatorcontrib><title>Upregulation of MiR-122 via Trichostatin A Treatments in Hepatocyte-like Cells Derived from Mesenchymal Stem Cells</title><title>Chemical biology & drug design</title><addtitle>Chem Biol Drug Des</addtitle><description>The miR‐122 is a tissue‐specific miRNA; its expression is abundant in liver. MiR‐122 upregulation is crucial for differentiation, functionality, and maintenance of differentiated phenotype in hepatocytes. The improving effects of trichostatin A (TSA) on hepatic differentiation have been reported previously. The aim of this study was to determine whether TSA can affect the expression of miR‐122 in hepatocyte‐like cells (HLCs) generated from human adipose tissue‐derived mesenchymal stem cells (hAT‐MSCs). The hepatic differentiation of hAT‐MSCs induced by a mixture of growth factors and cytokines either with or without TSA treatments. The functionality of HLCs generated with or without TSA and the expression levels of miR‐122 were studied. The expression levels of miR‐122 in TSA‐treated HLCs was significantly (p < 0.05) higher than those generated by growth factors and cytokines, only. The downregulation of a‐fetoprotein (AFP) levels but enhanced albumin synthesis (p < 0.05) and upregulation of liver‐enriched transcription factors (LETFs) HNF4α (hepatocyte nuclear factor 4α) and HNF6 (hepatocyte nuclear factor 6) were observed in TSA‐treated HLCs (p < 0.05). In conclusion, administration of TSA in hepatogenic differentiation of hAT‐MSCs resulted in higher expression levels of miR‐122, facilitation of differentiation, and subsequently attenuation of AFP levels.
Administration of TSA during hepatic differentiation of adipose tissue derived mesenchymal stem cells (AT‐MSCs) resulted in the facilitation of hepatic differentiation, higher miR‐ 122 expression levels, and subsequently attenuation of AFP expression in hepatocyte like cells.</description><subject>alpha-Fetoproteins - metabolism</subject><subject>Cell Differentiation - drug effects</subject><subject>Cell Lineage</subject><subject>Cells, Cultured</subject><subject>Down-Regulation - drug effects</subject><subject>Hepatocyte Nuclear Factor 4 - metabolism</subject><subject>Hepatocyte Nuclear Factor 6 - metabolism</subject><subject>hepatocyte-like cells</subject><subject>Hepatocytes - cytology</subject><subject>Hepatocytes - drug effects</subject><subject>Hepatocytes - metabolism</subject><subject>HNF4a</subject><subject>HNF6</subject><subject>Humans</subject><subject>Hydroxamic Acids - pharmacology</subject><subject>mesenchymal stem cells</subject><subject>Mesenchymal Stromal Cells - cytology</subject><subject>MicroRNAs - metabolism</subject><subject>miR-122</subject><subject>trichostatin A</subject><subject>Up-Regulation - drug effects</subject><subject>α-fetoprotein</subject><issn>1747-0277</issn><issn>1747-0285</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kElPHDEQha0oKCzhwg9APkZIDXZ76z6SmbAIhkgBQm6W264ODr1MbA8w_z49NDPH1KXqqb56Kj2EDig5pkOd2Mq5Y5pLyT-gHaq4ykheiI-bWalttBvjH0I4F3nxCW3nkklSMraDwv08wO9FY5LvO9zXeOZ_ZDTP8bM3-C54-9jHNCw7fDpIMKmFLkU86AuYm9TbZYKs8U-AJ9A0EU8h-GdwuA59i2cQobOPy9Y0-DZBOzKf0VZtmgj7730P3Z99u5tcZNffzy8np9eZZVLxTAhnTFU6TgtwUgkuQRDKHJG8cM4RUhJBTZVTJ5iria0VpcpUlhWVVRXL2R76MvrOQ_93ATHp1kc7fGA66BdRUyVJUXKh1IAejagNfYwBaj0PvjVhqSnRq4z1KmP9lvEAH777LqoW3AZdhzoAdARefAPL_1jpydfpdG2ajTc-Jnjd3JjwpKViSuiHm3P980H8IuXVTEv2D5aYlY0</recordid><startdate>201602</startdate><enddate>201602</enddate><creator>Alizadeh, Effat</creator><creator>Eslaminejad, MohamadReza Baghaban</creator><creator>Akbarzadeh, Abolfazl</creator><creator>Sadeghi, Zohre</creator><creator>Abasi, Mozghan</creator><creator>Herizchi, Roya</creator><creator>Zarghami, Nosratollah</creator><general>Blackwell Publishing Ltd</general><scope>BSCLL</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>7X8</scope></search><sort><creationdate>201602</creationdate><title>Upregulation of MiR-122 via Trichostatin A Treatments in Hepatocyte-like Cells Derived from Mesenchymal Stem Cells</title><author>Alizadeh, Effat ; Eslaminejad, MohamadReza Baghaban ; Akbarzadeh, Abolfazl ; Sadeghi, Zohre ; Abasi, Mozghan ; Herizchi, Roya ; Zarghami, Nosratollah</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3674-55daab9d418ed67546e5013d0648ddd009051ab21d53df0cf7117abc38bc7b323</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>alpha-Fetoproteins - metabolism</topic><topic>Cell Differentiation - drug effects</topic><topic>Cell Lineage</topic><topic>Cells, Cultured</topic><topic>Down-Regulation - drug effects</topic><topic>Hepatocyte Nuclear Factor 4 - metabolism</topic><topic>Hepatocyte Nuclear Factor 6 - metabolism</topic><topic>hepatocyte-like cells</topic><topic>Hepatocytes - cytology</topic><topic>Hepatocytes - drug effects</topic><topic>Hepatocytes - metabolism</topic><topic>HNF4a</topic><topic>HNF6</topic><topic>Humans</topic><topic>Hydroxamic Acids - pharmacology</topic><topic>mesenchymal stem cells</topic><topic>Mesenchymal Stromal Cells - cytology</topic><topic>MicroRNAs - metabolism</topic><topic>miR-122</topic><topic>trichostatin A</topic><topic>Up-Regulation - drug effects</topic><topic>α-fetoprotein</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Alizadeh, Effat</creatorcontrib><creatorcontrib>Eslaminejad, MohamadReza Baghaban</creatorcontrib><creatorcontrib>Akbarzadeh, Abolfazl</creatorcontrib><creatorcontrib>Sadeghi, Zohre</creatorcontrib><creatorcontrib>Abasi, Mozghan</creatorcontrib><creatorcontrib>Herizchi, Roya</creatorcontrib><creatorcontrib>Zarghami, Nosratollah</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Chemical biology & drug design</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Alizadeh, Effat</au><au>Eslaminejad, MohamadReza Baghaban</au><au>Akbarzadeh, Abolfazl</au><au>Sadeghi, Zohre</au><au>Abasi, Mozghan</au><au>Herizchi, Roya</au><au>Zarghami, Nosratollah</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Upregulation of MiR-122 via Trichostatin A Treatments in Hepatocyte-like Cells Derived from Mesenchymal Stem Cells</atitle><jtitle>Chemical biology & drug design</jtitle><addtitle>Chem Biol Drug Des</addtitle><date>2016-02</date><risdate>2016</risdate><volume>87</volume><issue>2</issue><spage>296</spage><epage>305</epage><pages>296-305</pages><issn>1747-0277</issn><eissn>1747-0285</eissn><abstract>The miR‐122 is a tissue‐specific miRNA; its expression is abundant in liver. MiR‐122 upregulation is crucial for differentiation, functionality, and maintenance of differentiated phenotype in hepatocytes. The improving effects of trichostatin A (TSA) on hepatic differentiation have been reported previously. The aim of this study was to determine whether TSA can affect the expression of miR‐122 in hepatocyte‐like cells (HLCs) generated from human adipose tissue‐derived mesenchymal stem cells (hAT‐MSCs). The hepatic differentiation of hAT‐MSCs induced by a mixture of growth factors and cytokines either with or without TSA treatments. The functionality of HLCs generated with or without TSA and the expression levels of miR‐122 were studied. The expression levels of miR‐122 in TSA‐treated HLCs was significantly (p < 0.05) higher than those generated by growth factors and cytokines, only. The downregulation of a‐fetoprotein (AFP) levels but enhanced albumin synthesis (p < 0.05) and upregulation of liver‐enriched transcription factors (LETFs) HNF4α (hepatocyte nuclear factor 4α) and HNF6 (hepatocyte nuclear factor 6) were observed in TSA‐treated HLCs (p < 0.05). In conclusion, administration of TSA in hepatogenic differentiation of hAT‐MSCs resulted in higher expression levels of miR‐122, facilitation of differentiation, and subsequently attenuation of AFP levels.
Administration of TSA during hepatic differentiation of adipose tissue derived mesenchymal stem cells (AT‐MSCs) resulted in the facilitation of hepatic differentiation, higher miR‐ 122 expression levels, and subsequently attenuation of AFP expression in hepatocyte like cells.</abstract><cop>England</cop><pub>Blackwell Publishing Ltd</pub><pmid>26360933</pmid><doi>10.1111/cbdd.12664</doi><tpages>10</tpages></addata></record> |
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subjects | alpha-Fetoproteins - metabolism Cell Differentiation - drug effects Cell Lineage Cells, Cultured Down-Regulation - drug effects Hepatocyte Nuclear Factor 4 - metabolism Hepatocyte Nuclear Factor 6 - metabolism hepatocyte-like cells Hepatocytes - cytology Hepatocytes - drug effects Hepatocytes - metabolism HNF4a HNF6 Humans Hydroxamic Acids - pharmacology mesenchymal stem cells Mesenchymal Stromal Cells - cytology MicroRNAs - metabolism miR-122 trichostatin A Up-Regulation - drug effects α-fetoprotein |
title | Upregulation of MiR-122 via Trichostatin A Treatments in Hepatocyte-like Cells Derived from Mesenchymal Stem Cells |
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