Clinical impact of serum exosomal microRNA in liver fibrosis
Background/aim We investigated alterations in the expression of serum exosomal miRNAs with the progression of liver fibrosis and evaluated their clinical applicability as biomarkers. Methods This study prospectively enrolled 71 patients who underwent liver biopsy at an academic hospital in Korea. Ex...
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| creator | Chang, Young Han, Jae-A Kang, Suk Min Jeong, Soung Won Ryu, Tom Park, Han Seul Yoo, Jeong-Ju Lee, Sae Hwan Kim, Sang Gyune Kim, Young Seok Kim, Hong Soo Jin, So Young Ryu, Seongho Jang, Jae Young |
| description | Background/aim We investigated alterations in the expression of serum exosomal miRNAs with the progression of liver fibrosis and evaluated their clinical applicability as biomarkers. Methods This study prospectively enrolled 71 patients who underwent liver biopsy at an academic hospital in Korea. Exosomes were extracted from serum samples, followed by next-generation sequencing (NGS) of miRNAs and targeted real-time quantitative polymerase chain reaction. A model was derived to discriminate advanced fibrosis based on miRNA levels and the performance of this model was evaluated. Validation of the effect of miRNA on liver fibrosis in vitro was followed. Results NGS data revealed that exosomal miR-660-5p, miR-125a-5p, and miR-122 expression were changed significantly with the progression of liver fibrosis, of which miR-122 exhibited high read counts enough to be used as a biomarker. The level of exosomal miR-122 decreased as the pathologic fibrosis grade progressed and patients with biopsy-proven advanced fibrosis had significantly lower levels of exosomal miR-122 (P < 0.001) than those without advanced fibrosis. Exosomal miR-122 exhibited a fair performance in discriminating advanced fibrosis especially in combination with fibrosis-4 score and transient elastography. In a subgroup of patients with a non-viral etiology of liver disease, the performance of exosomal miR-122 as a biomarker was greatly improved. Inhibition of miR-122 expression increased the proliferation of the human hepatic stellate cell line, LX-2, and upregulated the expression of various fibrosis related proteins. Conclusion Exosomal miR-122 may serve as a useful non-invasive biomarker for liver fibrosis, especially in patients with non-viral etiologies of chronic liver disease. |
| doi_str_mv | 10.1371/journal.pone.0255672 |
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Methods This study prospectively enrolled 71 patients who underwent liver biopsy at an academic hospital in Korea. Exosomes were extracted from serum samples, followed by next-generation sequencing (NGS) of miRNAs and targeted real-time quantitative polymerase chain reaction. A model was derived to discriminate advanced fibrosis based on miRNA levels and the performance of this model was evaluated. Validation of the effect of miRNA on liver fibrosis in vitro was followed. Results NGS data revealed that exosomal miR-660-5p, miR-125a-5p, and miR-122 expression were changed significantly with the progression of liver fibrosis, of which miR-122 exhibited high read counts enough to be used as a biomarker. The level of exosomal miR-122 decreased as the pathologic fibrosis grade progressed and patients with biopsy-proven advanced fibrosis had significantly lower levels of exosomal miR-122 (P < 0.001) than those without advanced fibrosis. Exosomal miR-122 exhibited a fair performance in discriminating advanced fibrosis especially in combination with fibrosis-4 score and transient elastography. In a subgroup of patients with a non-viral etiology of liver disease, the performance of exosomal miR-122 as a biomarker was greatly improved. Inhibition of miR-122 expression increased the proliferation of the human hepatic stellate cell line, LX-2, and upregulated the expression of various fibrosis related proteins. Conclusion Exosomal miR-122 may serve as a useful non-invasive biomarker for liver fibrosis, especially in patients with non-viral etiologies of chronic liver disease.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0255672</identifier><identifier>PMID: 34506494</identifier><language>eng</language><publisher>San Francisco: Public Library of Science</publisher><subject>Analysis ; Biology and life sciences ; Biomarkers ; Biopsy ; Care and treatment ; Communication ; Diagnosis ; Etiology ; Exosomes ; Fibrosis ; Gene expression ; Genomes ; Hepatitis ; Internal medicine ; Laboratories ; Liver ; Liver diseases ; Medical schools ; Medicine ; Medicine and Health Sciences ; Methods ; MicroRNA ; MicroRNAs ; miRNA ; Next-generation sequencing ; Patients ; Polymerase chain reaction ; Proteins ; Ribonucleic acid ; RNA ; Subgroups</subject><ispartof>PloS one, 2021-09, Vol.16 (9), p.e0255672-e0255672</ispartof><rights>COPYRIGHT 2021 Public Library of Science</rights><rights>2021 Chang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2021 Chang et al 2021 Chang et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c669t-a991f1b2ae8db351e691179373663f578c7ed5350c3f100bb9666989156eefb03</citedby><cites>FETCH-LOGICAL-c669t-a991f1b2ae8db351e691179373663f578c7ed5350c3f100bb9666989156eefb03</cites><orcidid>0000-0001-5335-752X</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/PMC8432846/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8432846/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,2928,23866,27924,27925,53791,53793</link.rule.ids></links><search><contributor>Mari, Bernard</contributor><creatorcontrib>Chang, Young</creatorcontrib><creatorcontrib>Han, Jae-A</creatorcontrib><creatorcontrib>Kang, Suk Min</creatorcontrib><creatorcontrib>Jeong, Soung Won</creatorcontrib><creatorcontrib>Ryu, Tom</creatorcontrib><creatorcontrib>Park, Han Seul</creatorcontrib><creatorcontrib>Yoo, Jeong-Ju</creatorcontrib><creatorcontrib>Lee, Sae Hwan</creatorcontrib><creatorcontrib>Kim, Sang Gyune</creatorcontrib><creatorcontrib>Kim, Young Seok</creatorcontrib><creatorcontrib>Kim, Hong Soo</creatorcontrib><creatorcontrib>Jin, So Young</creatorcontrib><creatorcontrib>Ryu, Seongho</creatorcontrib><creatorcontrib>Jang, Jae Young</creatorcontrib><title>Clinical impact of serum exosomal microRNA in liver fibrosis</title><title>PloS one</title><description>Background/aim We investigated alterations in the expression of serum exosomal miRNAs with the progression of liver fibrosis and evaluated their clinical applicability as biomarkers. Methods This study prospectively enrolled 71 patients who underwent liver biopsy at an academic hospital in Korea. Exosomes were extracted from serum samples, followed by next-generation sequencing (NGS) of miRNAs and targeted real-time quantitative polymerase chain reaction. A model was derived to discriminate advanced fibrosis based on miRNA levels and the performance of this model was evaluated. Validation of the effect of miRNA on liver fibrosis in vitro was followed. Results NGS data revealed that exosomal miR-660-5p, miR-125a-5p, and miR-122 expression were changed significantly with the progression of liver fibrosis, of which miR-122 exhibited high read counts enough to be used as a biomarker. The level of exosomal miR-122 decreased as the pathologic fibrosis grade progressed and patients with biopsy-proven advanced fibrosis had significantly lower levels of exosomal miR-122 (P < 0.001) than those without advanced fibrosis. Exosomal miR-122 exhibited a fair performance in discriminating advanced fibrosis especially in combination with fibrosis-4 score and transient elastography. In a subgroup of patients with a non-viral etiology of liver disease, the performance of exosomal miR-122 as a biomarker was greatly improved. Inhibition of miR-122 expression increased the proliferation of the human hepatic stellate cell line, LX-2, and upregulated the expression of various fibrosis related proteins. Conclusion Exosomal miR-122 may serve as a useful non-invasive biomarker for liver fibrosis, especially in patients with non-viral etiologies of chronic liver disease.</description><subject>Analysis</subject><subject>Biology and life sciences</subject><subject>Biomarkers</subject><subject>Biopsy</subject><subject>Care and treatment</subject><subject>Communication</subject><subject>Diagnosis</subject><subject>Etiology</subject><subject>Exosomes</subject><subject>Fibrosis</subject><subject>Gene expression</subject><subject>Genomes</subject><subject>Hepatitis</subject><subject>Internal medicine</subject><subject>Laboratories</subject><subject>Liver</subject><subject>Liver diseases</subject><subject>Medical schools</subject><subject>Medicine</subject><subject>Medicine and Health Sciences</subject><subject>Methods</subject><subject>MicroRNA</subject><subject>MicroRNAs</subject><subject>miRNA</subject><subject>Next-generation sequencing</subject><subject>Patients</subject><subject>Polymerase chain reaction</subject><subject>Proteins</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>Subgroups</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqNkl2LEzEUhgdR3LX6DwQHBNGL1mSSyQeIUIofhcWF9eM2ZDInbUpm0k1mlvXfm9pRtrIXkouEk-e8J-fkLYrnGC0w4fjtLoyx136xDz0sUFXXjFcPinMsSTVnFSIP75zPiicp7RCqiWDscXFGaI0YlfS8eLfyrndG-9J1e22GMtgyQRy7Em5DCl2-6JyJ4erLsnR96d0NxNK6Jobk0tPikdU-wbNpnxXfP374tvo8v7j8tF4tL-aGMTnMtZTY4qbSINqG1BiYxJhLwgljxNZcGA5tTWpkiMUINY1kOU9IXDMA2yAyK14cdfc-JDU1nlRVc0xpLbLUrFgfiTbondpH1-n4UwXt1O9AiBul4-CMB2UNxy1tKUhtaSW5BCEpsaihtJUW86z1fqo2Nh20Bvohan8ienrTu63ahBslKKkEZVng9SQQw_UIaVCdSwa81z2E8fhuiYUgJKMv_0Hv726iNjo34Hobcl1zEFVLxqlkQsrDlBb3UHm1kL8wu8S6HD9JeHOSkJkBboeNHlNS669X_89e_jhlX91ht6D9sE3Bj4MLfToF6RHMBkspgv07ZIzUweR_pqEOJleTyckvMjLrWw</recordid><startdate>20210910</startdate><enddate>20210910</enddate><creator>Chang, 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impact of serum exosomal microRNA in liver fibrosis</title><author>Chang, Young ; Han, Jae-A ; Kang, Suk Min ; Jeong, Soung Won ; Ryu, Tom ; Park, Han Seul ; Yoo, Jeong-Ju ; Lee, Sae Hwan ; Kim, Sang Gyune ; Kim, Young Seok ; Kim, Hong Soo ; Jin, So Young ; Ryu, Seongho ; Jang, Jae Young</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c669t-a991f1b2ae8db351e691179373663f578c7ed5350c3f100bb9666989156eefb03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Analysis</topic><topic>Biology and life sciences</topic><topic>Biomarkers</topic><topic>Biopsy</topic><topic>Care and treatment</topic><topic>Communication</topic><topic>Diagnosis</topic><topic>Etiology</topic><topic>Exosomes</topic><topic>Fibrosis</topic><topic>Gene expression</topic><topic>Genomes</topic><topic>Hepatitis</topic><topic>Internal medicine</topic><topic>Laboratories</topic><topic>Liver</topic><topic>Liver diseases</topic><topic>Medical schools</topic><topic>Medicine</topic><topic>Medicine and Health Sciences</topic><topic>Methods</topic><topic>MicroRNA</topic><topic>MicroRNAs</topic><topic>miRNA</topic><topic>Next-generation sequencing</topic><topic>Patients</topic><topic>Polymerase chain reaction</topic><topic>Proteins</topic><topic>Ribonucleic acid</topic><topic>RNA</topic><topic>Subgroups</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chang, Young</creatorcontrib><creatorcontrib>Han, Jae-A</creatorcontrib><creatorcontrib>Kang, Suk Min</creatorcontrib><creatorcontrib>Jeong, Soung Won</creatorcontrib><creatorcontrib>Ryu, Tom</creatorcontrib><creatorcontrib>Park, Han Seul</creatorcontrib><creatorcontrib>Yoo, Jeong-Ju</creatorcontrib><creatorcontrib>Lee, Sae Hwan</creatorcontrib><creatorcontrib>Kim, Sang Gyune</creatorcontrib><creatorcontrib>Kim, Young Seok</creatorcontrib><creatorcontrib>Kim, Hong Soo</creatorcontrib><creatorcontrib>Jin, So 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Bernard</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Clinical impact of serum exosomal microRNA in liver fibrosis</atitle><jtitle>PloS one</jtitle><date>2021-09-10</date><risdate>2021</risdate><volume>16</volume><issue>9</issue><spage>e0255672</spage><epage>e0255672</epage><pages>e0255672-e0255672</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Background/aim We investigated alterations in the expression of serum exosomal miRNAs with the progression of liver fibrosis and evaluated their clinical applicability as biomarkers. Methods This study prospectively enrolled 71 patients who underwent liver biopsy at an academic hospital in Korea. Exosomes were extracted from serum samples, followed by next-generation sequencing (NGS) of miRNAs and targeted real-time quantitative polymerase chain reaction. A model was derived to discriminate advanced fibrosis based on miRNA levels and the performance of this model was evaluated. Validation of the effect of miRNA on liver fibrosis in vitro was followed. Results NGS data revealed that exosomal miR-660-5p, miR-125a-5p, and miR-122 expression were changed significantly with the progression of liver fibrosis, of which miR-122 exhibited high read counts enough to be used as a biomarker. The level of exosomal miR-122 decreased as the pathologic fibrosis grade progressed and patients with biopsy-proven advanced fibrosis had significantly lower levels of exosomal miR-122 (P < 0.001) than those without advanced fibrosis. Exosomal miR-122 exhibited a fair performance in discriminating advanced fibrosis especially in combination with fibrosis-4 score and transient elastography. In a subgroup of patients with a non-viral etiology of liver disease, the performance of exosomal miR-122 as a biomarker was greatly improved. Inhibition of miR-122 expression increased the proliferation of the human hepatic stellate cell line, LX-2, and upregulated the expression of various fibrosis related proteins. Conclusion Exosomal miR-122 may serve as a useful non-invasive biomarker for liver fibrosis, especially in patients with non-viral etiologies of chronic liver disease.</abstract><cop>San Francisco</cop><pub>Public Library of Science</pub><pmid>34506494</pmid><doi>10.1371/journal.pone.0255672</doi><tpages>e0255672</tpages><orcidid>https://orcid.org/0000-0001-5335-752X</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Analysis Biology and life sciences Biomarkers Biopsy Care and treatment Communication Diagnosis Etiology Exosomes Fibrosis Gene expression Genomes Hepatitis Internal medicine Laboratories Liver Liver diseases Medical schools Medicine Medicine and Health Sciences Methods MicroRNA MicroRNAs miRNA Next-generation sequencing Patients Polymerase chain reaction Proteins Ribonucleic acid RNA Subgroups |
| title | Clinical impact of serum exosomal microRNA in liver fibrosis |
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