MiR‐122 modification enhances the therapeutic efficacy of adipose tissue‐derived mesenchymal stem cells against liver fibrosis
Mesenchymal stem cell (MSC) transplantation alone may be insufficient for treatment of liver fibrosis because of complicated histopathological changes in the liver. Given that miR‐122 plays an essential role in liver fibrosis by negatively regulating the proliferation and transactivation of hepatic...
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| Veröffentlicht in: | Journal of cellular and molecular medicine 2017-11, Vol.21 (11), p.2963-2973 |
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| creator | Lou, Guohua Yang, Ying Liu, Feifei Ye, Bingjue Chen, Zhi Zheng, Min Liu, Yanning |
| description | Mesenchymal stem cell (MSC) transplantation alone may be insufficient for treatment of liver fibrosis because of complicated histopathological changes in the liver. Given that miR‐122 plays an essential role in liver fibrosis by negatively regulating the proliferation and transactivation of hepatic stellate cells (HSCs), this study investigated whether miR‐122 modification can improve the therapeutic efficacy of adipose tissue‐derived MSCs in treating liver fibrosis. MiR‐122‐modified AMSCs (AMSC‐122) were constructed through lentivirus‐mediated transfer of pre‐miR‐122. MiR‐122‐modified AMSCs expressed high level of miR‐122, while they retained their phenotype and differentiation potential as naïve AMSCs. AMSC‐122 more effectively suppressed the proliferation of and collagen maturation in HSCs than scramble miRNA‐modified AMSCs. In addition, AMSC‐derived exosomes mediated the miR‐122 communication between AMSCs and HSCs, further affecting the expression levels of miR‐122 target genes, such as insulin‐like growth factor receptor 1 (IGF1R), Cyclin G(1) (CCNG1) and prolyl‐4‐hydroxylase α1 (P4HA1), which are involved in proliferation of and collagen maturation in HSCs. Moreover, miR‐122 modification enhanced the therapeutic efficacy of AMSCs in the treatment of carbon tetrachloride (CCl4)‐induced liver fibrosis by suppressing the activation of HSCs and alleviating collagen deposition. Results demonstrate that miR‐122 modification improves the therapeutic efficacy of AMSCs through exosome‐mediated miR‐122 communication; thus, miR‐122 modification is a new potential strategy for treatment of liver fibrosis. |
| doi_str_mv | 10.1111/jcmm.13208 |
| format | Article |
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Given that miR‐122 plays an essential role in liver fibrosis by negatively regulating the proliferation and transactivation of hepatic stellate cells (HSCs), this study investigated whether miR‐122 modification can improve the therapeutic efficacy of adipose tissue‐derived MSCs in treating liver fibrosis. MiR‐122‐modified AMSCs (AMSC‐122) were constructed through lentivirus‐mediated transfer of pre‐miR‐122. MiR‐122‐modified AMSCs expressed high level of miR‐122, while they retained their phenotype and differentiation potential as naïve AMSCs. AMSC‐122 more effectively suppressed the proliferation of and collagen maturation in HSCs than scramble miRNA‐modified AMSCs. In addition, AMSC‐derived exosomes mediated the miR‐122 communication between AMSCs and HSCs, further affecting the expression levels of miR‐122 target genes, such as insulin‐like growth factor receptor 1 (IGF1R), Cyclin G(1) (CCNG1) and prolyl‐4‐hydroxylase α1 (P4HA1), which are involved in proliferation of and collagen maturation in HSCs. Moreover, miR‐122 modification enhanced the therapeutic efficacy of AMSCs in the treatment of carbon tetrachloride (CCl4)‐induced liver fibrosis by suppressing the activation of HSCs and alleviating collagen deposition. Results demonstrate that miR‐122 modification improves the therapeutic efficacy of AMSCs through exosome‐mediated miR‐122 communication; thus, miR‐122 modification is a new potential strategy for treatment of liver fibrosis.</description><identifier>ISSN: 1582-1838</identifier><identifier>EISSN: 1582-4934</identifier><identifier>DOI: 10.1111/jcmm.13208</identifier><identifier>PMID: 28544786</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>Adipose tissue ; Adipose Tissue - cytology ; Adipose Tissue - metabolism ; adipose tissue‐derived mesenchymal stem cells ; Animals ; Bile ; Body fat ; Carbon Tetrachloride ; Cell Communication ; Cell Cycle - genetics ; Cell Differentiation ; Cell Engineering ; Cell Proliferation ; Collagen ; Cyclin G ; Cyclin G1 - genetics ; Cyclin G1 - metabolism ; exosome ; Exosomes ; Exosomes - metabolism ; Fibrosis ; Gene Expression Regulation ; hepatic stellate cells ; Hepatic Stellate Cells - metabolism ; Hepatic Stellate Cells - pathology ; Hepatocytes ; Hydroxylase ; Insulin ; Insulin-like growth factor I receptors ; Liver ; Liver Cirrhosis - chemically induced ; Liver Cirrhosis - genetics ; Liver Cirrhosis - pathology ; Liver Cirrhosis - therapy ; liver fibrosis ; Mesenchymal Stem Cell Transplantation ; Mesenchymal stem cells ; Mesenchymal Stromal Cells - cytology ; Mesenchymal Stromal Cells - metabolism ; Mesenchyme ; Mice ; Mice, Inbred C57BL ; MicroRNAs - genetics ; MicroRNAs - metabolism ; miRNA ; miR‐122 ; Original ; Primary Cell Culture ; Prolyl Hydroxylases - genetics ; Prolyl Hydroxylases - metabolism ; Receptor, IGF Type 1 - genetics ; Receptor, IGF Type 1 - metabolism ; Signal Transduction ; Stellate cells ; Stem cells ; Transplantation</subject><ispartof>Journal of cellular and molecular medicine, 2017-11, Vol.21 (11), p.2963-2973</ispartof><rights>2017 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.</rights><rights>2017. 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><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5148-4e52d542f207d5ce3ebc96b51d5ecba29eaa8221586005e49d32551fa35f788c3</citedby><cites>FETCH-LOGICAL-c5148-4e52d542f207d5ce3ebc96b51d5ecba29eaa8221586005e49d32551fa35f788c3</cites><orcidid>0000-0002-0554-6622</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5661245/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5661245/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,728,781,785,865,886,1418,11567,27929,27930,45579,45580,46057,46481,53796,53798</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28544786$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lou, Guohua</creatorcontrib><creatorcontrib>Yang, Ying</creatorcontrib><creatorcontrib>Liu, Feifei</creatorcontrib><creatorcontrib>Ye, Bingjue</creatorcontrib><creatorcontrib>Chen, Zhi</creatorcontrib><creatorcontrib>Zheng, Min</creatorcontrib><creatorcontrib>Liu, Yanning</creatorcontrib><title>MiR‐122 modification enhances the therapeutic efficacy of adipose tissue‐derived mesenchymal stem cells against liver fibrosis</title><title>Journal of cellular and molecular medicine</title><addtitle>J Cell Mol Med</addtitle><description>Mesenchymal stem cell (MSC) transplantation alone may be insufficient for treatment of liver fibrosis because of complicated histopathological changes in the liver. Given that miR‐122 plays an essential role in liver fibrosis by negatively regulating the proliferation and transactivation of hepatic stellate cells (HSCs), this study investigated whether miR‐122 modification can improve the therapeutic efficacy of adipose tissue‐derived MSCs in treating liver fibrosis. MiR‐122‐modified AMSCs (AMSC‐122) were constructed through lentivirus‐mediated transfer of pre‐miR‐122. MiR‐122‐modified AMSCs expressed high level of miR‐122, while they retained their phenotype and differentiation potential as naïve AMSCs. AMSC‐122 more effectively suppressed the proliferation of and collagen maturation in HSCs than scramble miRNA‐modified AMSCs. In addition, AMSC‐derived exosomes mediated the miR‐122 communication between AMSCs and HSCs, further affecting the expression levels of miR‐122 target genes, such as insulin‐like growth factor receptor 1 (IGF1R), Cyclin G(1) (CCNG1) and prolyl‐4‐hydroxylase α1 (P4HA1), which are involved in proliferation of and collagen maturation in HSCs. Moreover, miR‐122 modification enhanced the therapeutic efficacy of AMSCs in the treatment of carbon tetrachloride (CCl4)‐induced liver fibrosis by suppressing the activation of HSCs and alleviating collagen deposition. Results demonstrate that miR‐122 modification improves the therapeutic efficacy of AMSCs through exosome‐mediated miR‐122 communication; thus, miR‐122 modification is a new potential strategy for treatment of liver fibrosis.</description><subject>Adipose tissue</subject><subject>Adipose Tissue - cytology</subject><subject>Adipose Tissue - metabolism</subject><subject>adipose tissue‐derived mesenchymal stem cells</subject><subject>Animals</subject><subject>Bile</subject><subject>Body fat</subject><subject>Carbon Tetrachloride</subject><subject>Cell Communication</subject><subject>Cell Cycle - genetics</subject><subject>Cell Differentiation</subject><subject>Cell Engineering</subject><subject>Cell Proliferation</subject><subject>Collagen</subject><subject>Cyclin G</subject><subject>Cyclin G1 - genetics</subject><subject>Cyclin G1 - metabolism</subject><subject>exosome</subject><subject>Exosomes</subject><subject>Exosomes - metabolism</subject><subject>Fibrosis</subject><subject>Gene Expression Regulation</subject><subject>hepatic stellate cells</subject><subject>Hepatic Stellate Cells - metabolism</subject><subject>Hepatic Stellate Cells - pathology</subject><subject>Hepatocytes</subject><subject>Hydroxylase</subject><subject>Insulin</subject><subject>Insulin-like growth factor I receptors</subject><subject>Liver</subject><subject>Liver Cirrhosis - chemically induced</subject><subject>Liver Cirrhosis - genetics</subject><subject>Liver Cirrhosis - pathology</subject><subject>Liver Cirrhosis - therapy</subject><subject>liver fibrosis</subject><subject>Mesenchymal Stem Cell Transplantation</subject><subject>Mesenchymal stem cells</subject><subject>Mesenchymal Stromal Cells - cytology</subject><subject>Mesenchymal Stromal Cells - metabolism</subject><subject>Mesenchyme</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>miRNA</subject><subject>miR‐122</subject><subject>Original</subject><subject>Primary Cell Culture</subject><subject>Prolyl Hydroxylases - genetics</subject><subject>Prolyl Hydroxylases - metabolism</subject><subject>Receptor, IGF Type 1 - genetics</subject><subject>Receptor, IGF Type 1 - metabolism</subject><subject>Signal Transduction</subject><subject>Stellate cells</subject><subject>Stem cells</subject><subject>Transplantation</subject><issn>1582-1838</issn><issn>1582-4934</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>WIN</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kd9qFDEUh4MotlZvfAAJeCOFrfk7k7kRZLFa6SKIXodM5kw3yyRZk5nK3pU-gc_ok5jprkW9MBBy4Hx8nJMfQs8pOaPlvN5Y788oZ0Q9QMdUKrYQDRcPDzVVXB2hJzlvCOEV5c1jdMSUFKJW1TG6XbnPP29-UMawj53rnTWjiwFDWJtgIeNxDfNNZgvT6CyGfmbsDscem85tYy59l_MERdNBctfQYQ8Zgl3vvBlwHsFjC8OQsbkyLuQRDwVKuHdtitnlp-hRb4YMzw7vCfp6_u7L8sPi8tP7i-Xby4WVVKiFAMk6KVjPSN1JCxxa21StpJ0E2xrWgDGKsbJzRYgE0XScSUl7w2VfK2X5CXqz926n1kNnIYzJDHqbnDdpp6Nx-u9OcGt9Fa-1rCrKhCyCVwdBit8myKP2Ls-bmQBxypo2hNOK1YwX9OU_6CZOKZT1CiVropqK0kKd7ilbPiIn6O-HoUTP0eo5Wn0XbYFf_Dn-Pfo7ywLQPfDdDbD7j0p_XK5We-kvxzezPQ</recordid><startdate>201711</startdate><enddate>201711</enddate><creator>Lou, Guohua</creator><creator>Yang, Ying</creator><creator>Liu, Feifei</creator><creator>Ye, Bingjue</creator><creator>Chen, Zhi</creator><creator>Zheng, Min</creator><creator>Liu, Yanning</creator><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</scope><scope>WIN</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>3V.</scope><scope>7QP</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-0554-6622</orcidid></search><sort><creationdate>201711</creationdate><title>MiR‐122 modification enhances the therapeutic efficacy of adipose tissue‐derived mesenchymal stem cells against liver fibrosis</title><author>Lou, Guohua ; Yang, Ying ; Liu, Feifei ; Ye, Bingjue ; Chen, Zhi ; Zheng, Min ; Liu, Yanning</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5148-4e52d542f207d5ce3ebc96b51d5ecba29eaa8221586005e49d32551fa35f788c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Adipose tissue</topic><topic>Adipose Tissue - cytology</topic><topic>Adipose Tissue - metabolism</topic><topic>adipose tissue‐derived mesenchymal stem cells</topic><topic>Animals</topic><topic>Bile</topic><topic>Body fat</topic><topic>Carbon Tetrachloride</topic><topic>Cell Communication</topic><topic>Cell Cycle - genetics</topic><topic>Cell Differentiation</topic><topic>Cell Engineering</topic><topic>Cell Proliferation</topic><topic>Collagen</topic><topic>Cyclin G</topic><topic>Cyclin G1 - genetics</topic><topic>Cyclin G1 - metabolism</topic><topic>exosome</topic><topic>Exosomes</topic><topic>Exosomes - metabolism</topic><topic>Fibrosis</topic><topic>Gene Expression Regulation</topic><topic>hepatic stellate cells</topic><topic>Hepatic Stellate Cells - metabolism</topic><topic>Hepatic Stellate Cells - pathology</topic><topic>Hepatocytes</topic><topic>Hydroxylase</topic><topic>Insulin</topic><topic>Insulin-like growth factor I receptors</topic><topic>Liver</topic><topic>Liver Cirrhosis - chemically induced</topic><topic>Liver Cirrhosis - genetics</topic><topic>Liver Cirrhosis - pathology</topic><topic>Liver Cirrhosis - therapy</topic><topic>liver fibrosis</topic><topic>Mesenchymal Stem Cell Transplantation</topic><topic>Mesenchymal stem cells</topic><topic>Mesenchymal Stromal Cells - cytology</topic><topic>Mesenchymal Stromal Cells - metabolism</topic><topic>Mesenchyme</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>miRNA</topic><topic>miR‐122</topic><topic>Original</topic><topic>Primary Cell Culture</topic><topic>Prolyl Hydroxylases - genetics</topic><topic>Prolyl Hydroxylases - metabolism</topic><topic>Receptor, IGF Type 1 - genetics</topic><topic>Receptor, IGF Type 1 - metabolism</topic><topic>Signal Transduction</topic><topic>Stellate cells</topic><topic>Stem cells</topic><topic>Transplantation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lou, Guohua</creatorcontrib><creatorcontrib>Yang, Ying</creatorcontrib><creatorcontrib>Liu, Feifei</creatorcontrib><creatorcontrib>Ye, Bingjue</creatorcontrib><creatorcontrib>Chen, Zhi</creatorcontrib><creatorcontrib>Zheng, Min</creatorcontrib><creatorcontrib>Liu, Yanning</creatorcontrib><collection>Wiley Online Library (Open Access Collection)</collection><collection>Wiley Online Library (Open Access Collection)</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Publicly Available Content Database</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 China</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of cellular and molecular medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lou, Guohua</au><au>Yang, Ying</au><au>Liu, Feifei</au><au>Ye, Bingjue</au><au>Chen, Zhi</au><au>Zheng, Min</au><au>Liu, Yanning</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>MiR‐122 modification enhances the therapeutic efficacy of adipose tissue‐derived mesenchymal stem cells against liver fibrosis</atitle><jtitle>Journal of cellular and molecular medicine</jtitle><addtitle>J Cell Mol Med</addtitle><date>2017-11</date><risdate>2017</risdate><volume>21</volume><issue>11</issue><spage>2963</spage><epage>2973</epage><pages>2963-2973</pages><issn>1582-1838</issn><eissn>1582-4934</eissn><abstract>Mesenchymal stem cell (MSC) transplantation alone may be insufficient for treatment of liver fibrosis because of complicated histopathological changes in the liver. Given that miR‐122 plays an essential role in liver fibrosis by negatively regulating the proliferation and transactivation of hepatic stellate cells (HSCs), this study investigated whether miR‐122 modification can improve the therapeutic efficacy of adipose tissue‐derived MSCs in treating liver fibrosis. MiR‐122‐modified AMSCs (AMSC‐122) were constructed through lentivirus‐mediated transfer of pre‐miR‐122. MiR‐122‐modified AMSCs expressed high level of miR‐122, while they retained their phenotype and differentiation potential as naïve AMSCs. AMSC‐122 more effectively suppressed the proliferation of and collagen maturation in HSCs than scramble miRNA‐modified AMSCs. In addition, AMSC‐derived exosomes mediated the miR‐122 communication between AMSCs and HSCs, further affecting the expression levels of miR‐122 target genes, such as insulin‐like growth factor receptor 1 (IGF1R), Cyclin G(1) (CCNG1) and prolyl‐4‐hydroxylase α1 (P4HA1), which are involved in proliferation of and collagen maturation in HSCs. Moreover, miR‐122 modification enhanced the therapeutic efficacy of AMSCs in the treatment of carbon tetrachloride (CCl4)‐induced liver fibrosis by suppressing the activation of HSCs and alleviating collagen deposition. Results demonstrate that miR‐122 modification improves the therapeutic efficacy of AMSCs through exosome‐mediated miR‐122 communication; thus, miR‐122 modification is a new potential strategy for treatment of liver fibrosis.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>28544786</pmid><doi>10.1111/jcmm.13208</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0002-0554-6622</orcidid><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; DOAJ Directory of Open Access Journals; Access via Wiley Online Library; EZB-FREE-00999 freely available EZB journals; Wiley Online Library (Open Access Collection); PubMed Central |
| subjects | Adipose tissue Adipose Tissue - cytology Adipose Tissue - metabolism adipose tissue‐derived mesenchymal stem cells Animals Bile Body fat Carbon Tetrachloride Cell Communication Cell Cycle - genetics Cell Differentiation Cell Engineering Cell Proliferation Collagen Cyclin G Cyclin G1 - genetics Cyclin G1 - metabolism exosome Exosomes Exosomes - metabolism Fibrosis Gene Expression Regulation hepatic stellate cells Hepatic Stellate Cells - metabolism Hepatic Stellate Cells - pathology Hepatocytes Hydroxylase Insulin Insulin-like growth factor I receptors Liver Liver Cirrhosis - chemically induced Liver Cirrhosis - genetics Liver Cirrhosis - pathology Liver Cirrhosis - therapy liver fibrosis Mesenchymal Stem Cell Transplantation Mesenchymal stem cells Mesenchymal Stromal Cells - cytology Mesenchymal Stromal Cells - metabolism Mesenchyme Mice Mice, Inbred C57BL MicroRNAs - genetics MicroRNAs - metabolism miRNA miR‐122 Original Primary Cell Culture Prolyl Hydroxylases - genetics Prolyl Hydroxylases - metabolism Receptor, IGF Type 1 - genetics Receptor, IGF Type 1 - metabolism Signal Transduction Stellate cells Stem cells Transplantation |
| title | MiR‐122 modification enhances the therapeutic efficacy of adipose tissue‐derived mesenchymal stem cells against liver fibrosis |
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