Partial Hepatectomy-Induced Upregulation of miR-1907 Accelerates Liver Regeneration by Activation Autophagy
Liver regeneration after partial hepatectomy (PH) is a highly orchestrated biological process in which synchronized hepatocyte proliferation is induced after massive liver mass loss. Hepatocyte proliferation could be regulated by multiple signals, such as miRNAs and autophagy, but underlying mechani...
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description | Liver regeneration after partial hepatectomy (PH) is a highly orchestrated biological process in which synchronized hepatocyte proliferation is induced after massive liver mass loss. Hepatocyte proliferation could be regulated by multiple signals, such as miRNAs and autophagy, but underlying mechanism remains unclear. Here a functional miRNA during liver regeneration was identified and its underlying mechanism was delineated in vitro and in vivo. We found that miR-1907 was highly upregulated during liver regeneration after 2/3 PH at various timepoints. The level of miR-1907 was also increased in normal liver cell line treated with HGF at different concentrations. Functionally, miR-1907 enhanced hepatocyte proliferation in vitro and in vivo, and the liver/body weight ratio in miR-1907-overexpressed mice was significantly higher in comparison to the control mice after 2/3 PH. Forced expression of miR-1907 promoted autophagy activation of hepatocyte. Importantly, autophagy inhibition significantly attenuated miR-1907-induced hepatocyte proliferation and the liver/body weight ratio. Finally, GSK3β, a suppressor of autophagy signaling, was identified as the direct target gene of miR-1907. Taken together, miR-1907 accelerates hepatocyte proliferation during liver regeneration by activating autophagy; thus pharmacological intervention regulating miR-1907/autophagy axis may be therapeutically beneficial in liver transplantation and liver failure by inducing liver regeneration. |
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Hepatocyte proliferation could be regulated by multiple signals, such as miRNAs and autophagy, but underlying mechanism remains unclear. Here a functional miRNA during liver regeneration was identified and its underlying mechanism was delineated in vitro and in vivo. We found that miR-1907 was highly upregulated during liver regeneration after 2/3 PH at various timepoints. The level of miR-1907 was also increased in normal liver cell line treated with HGF at different concentrations. Functionally, miR-1907 enhanced hepatocyte proliferation in vitro and in vivo, and the liver/body weight ratio in miR-1907-overexpressed mice was significantly higher in comparison to the control mice after 2/3 PH. Forced expression of miR-1907 promoted autophagy activation of hepatocyte. Importantly, autophagy inhibition significantly attenuated miR-1907-induced hepatocyte proliferation and the liver/body weight ratio. Finally, GSK3β, a suppressor of autophagy signaling, was identified as the direct target gene of miR-1907. Taken together, miR-1907 accelerates hepatocyte proliferation during liver regeneration by activating autophagy; thus pharmacological intervention regulating miR-1907/autophagy axis may be therapeutically beneficial in liver transplantation and liver failure by inducing liver regeneration.</description><identifier>ISSN: 2314-6133</identifier><identifier>EISSN: 2314-6141</identifier><identifier>DOI: 10.1155/2018/3817057</identifier><identifier>PMID: 30151380</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>Activation ; Analysis ; Animals ; Apoptosis ; Autophagy ; Biological activity ; Body weight ; Cell Proliferation ; China ; Growth factors ; Hepatectomy ; Hepatocytes ; Hepatology ; Laboratories ; Liver ; Liver cancer ; Liver diseases ; Liver Regeneration ; Liver transplantation ; Mice ; Mice, Inbred C57BL ; MicroRNA ; MicroRNAs ; MicroRNAs - metabolism ; miRNA ; Mutation ; Phagocytosis ; Pharmacology ; Regeneration ; Target recognition ; Transplantation ; Transplantation of organs, tissues, etc ; Up-Regulation</subject><ispartof>BioMed research international, 2018-01, Vol.2018 (2018), p.1-9</ispartof><rights>Copyright © 2018 Tianfei Lu et al.</rights><rights>COPYRIGHT 2018 John Wiley & Sons, Inc.</rights><rights>Copyright © 2018 Tianfei Lu et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. https://creativecommons.org/licenses/by/4.0</rights><rights>Copyright © 2018 Tianfei Lu et al. 2018</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c499t-dc7952f7b6ed5dc593ec415105d92cd4509954fd171b913aea04a7d79e606c1a3</citedby><cites>FETCH-LOGICAL-c499t-dc7952f7b6ed5dc593ec415105d92cd4509954fd171b913aea04a7d79e606c1a3</cites><orcidid>0000-0002-2912-6016</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/PMC6091409/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6091409/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30151380$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Li, Kui</contributor><creatorcontrib>Zhang, Jianjun</creatorcontrib><creatorcontrib>Gu, Guangxiang</creatorcontrib><creatorcontrib>Shen, Chuan</creatorcontrib><creatorcontrib>Hao, Jun</creatorcontrib><creatorcontrib>Lu, Tianfei</creatorcontrib><creatorcontrib>Xu, Ning</creatorcontrib><title>Partial Hepatectomy-Induced Upregulation of miR-1907 Accelerates Liver Regeneration by Activation Autophagy</title><title>BioMed research international</title><addtitle>Biomed Res Int</addtitle><description>Liver regeneration after partial hepatectomy (PH) is a highly orchestrated biological process in which synchronized hepatocyte proliferation is induced after massive liver mass loss. Hepatocyte proliferation could be regulated by multiple signals, such as miRNAs and autophagy, but underlying mechanism remains unclear. Here a functional miRNA during liver regeneration was identified and its underlying mechanism was delineated in vitro and in vivo. We found that miR-1907 was highly upregulated during liver regeneration after 2/3 PH at various timepoints. The level of miR-1907 was also increased in normal liver cell line treated with HGF at different concentrations. Functionally, miR-1907 enhanced hepatocyte proliferation in vitro and in vivo, and the liver/body weight ratio in miR-1907-overexpressed mice was significantly higher in comparison to the control mice after 2/3 PH. Forced expression of miR-1907 promoted autophagy activation of hepatocyte. Importantly, autophagy inhibition significantly attenuated miR-1907-induced hepatocyte proliferation and the liver/body weight ratio. Finally, GSK3β, a suppressor of autophagy signaling, was identified as the direct target gene of miR-1907. Taken together, miR-1907 accelerates hepatocyte proliferation during liver regeneration by activating autophagy; thus pharmacological intervention regulating miR-1907/autophagy axis may be therapeutically beneficial in liver transplantation and liver failure by inducing liver regeneration.</description><subject>Activation</subject><subject>Analysis</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Autophagy</subject><subject>Biological activity</subject><subject>Body weight</subject><subject>Cell Proliferation</subject><subject>China</subject><subject>Growth factors</subject><subject>Hepatectomy</subject><subject>Hepatocytes</subject><subject>Hepatology</subject><subject>Laboratories</subject><subject>Liver</subject><subject>Liver cancer</subject><subject>Liver diseases</subject><subject>Liver Regeneration</subject><subject>Liver transplantation</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>MicroRNA</subject><subject>MicroRNAs</subject><subject>MicroRNAs - metabolism</subject><subject>miRNA</subject><subject>Mutation</subject><subject>Phagocytosis</subject><subject>Pharmacology</subject><subject>Regeneration</subject><subject>Target recognition</subject><subject>Transplantation</subject><subject>Transplantation of organs, tissues, etc</subject><subject>Up-Regulation</subject><issn>2314-6133</issn><issn>2314-6141</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqNkc1v1DAQxS0EolXpjTOKxAUJQj1x7MQXpFUFtNJKoIqeLa89ybokcXCcRfvf42iXLXDCF3_95vmNHyEvgb4H4PyqoFBfsRoqyqsn5LxgUOYCSnh6WjN2Ri6n6YGmUYOgUjwnZ4wCB1bTc_L9qw7R6S67wVFHNNH3-_x2sLNBm92PAdu509H5IfNN1ru7HCStspUx2GFIBVO2djsM2R22OCwnC7rZJyK63WG3mqMft7rdvyDPGt1NeHmcL8j9p4_frm_y9ZfPt9erdW5KKWNuTSV50VQbgZZbwyVDUya_lFtZGFtyKiUvGwsVbCQwjZqWurKVREGFAc0uyIeD7jhverQGhxh0p8bgeh32ymun_r4Z3Fa1fqfS70BJZRJ4cxQI_seMU1S9m1LHnR7Qz5MqqOS8EILXCX39D_rg5zCk9hJVVxxqwcpHqtUdKjc0Pr1rFlG1EgXUlEIhEvXuQJngpylgc7IMVC1xqyVudYw74a_-bPME_w43AW8PwNYNVv90_ymHicFGP9LJGxSM_QKmSbrY</recordid><startdate>20180101</startdate><enddate>20180101</enddate><creator>Zhang, Jianjun</creator><creator>Gu, Guangxiang</creator><creator>Shen, Chuan</creator><creator>Hao, Jun</creator><creator>Lu, Tianfei</creator><creator>Xu, Ning</creator><general>Hindawi Publishing Corporation</general><general>Hindawi</general><general>John Wiley & Sons, Inc</general><general>Hindawi Limited</general><scope>ADJCN</scope><scope>AHFXO</scope><scope>RHU</scope><scope>RHW</scope><scope>RHX</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>7QL</scope><scope>7QO</scope><scope>7T7</scope><scope>7TK</scope><scope>7U7</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>CWDGH</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PHGZM</scope><scope>PHGZT</scope><scope>PIMPY</scope><scope>PJZUB</scope><scope>PKEHL</scope><scope>PPXIY</scope><scope>PQEST</scope><scope>PQGLB</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-2912-6016</orcidid></search><sort><creationdate>20180101</creationdate><title>Partial Hepatectomy-Induced Upregulation of miR-1907 Accelerates Liver Regeneration by Activation Autophagy</title><author>Zhang, Jianjun ; Gu, Guangxiang ; Shen, Chuan ; Hao, Jun ; Lu, Tianfei ; Xu, Ning</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c499t-dc7952f7b6ed5dc593ec415105d92cd4509954fd171b913aea04a7d79e606c1a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Activation</topic><topic>Analysis</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Autophagy</topic><topic>Biological activity</topic><topic>Body weight</topic><topic>Cell Proliferation</topic><topic>China</topic><topic>Growth factors</topic><topic>Hepatectomy</topic><topic>Hepatocytes</topic><topic>Hepatology</topic><topic>Laboratories</topic><topic>Liver</topic><topic>Liver cancer</topic><topic>Liver diseases</topic><topic>Liver Regeneration</topic><topic>Liver transplantation</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>MicroRNA</topic><topic>MicroRNAs</topic><topic>MicroRNAs - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>BioMed research international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Jianjun</au><au>Gu, Guangxiang</au><au>Shen, Chuan</au><au>Hao, Jun</au><au>Lu, Tianfei</au><au>Xu, Ning</au><au>Li, Kui</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Partial Hepatectomy-Induced Upregulation of miR-1907 Accelerates Liver Regeneration by Activation Autophagy</atitle><jtitle>BioMed research international</jtitle><addtitle>Biomed Res Int</addtitle><date>2018-01-01</date><risdate>2018</risdate><volume>2018</volume><issue>2018</issue><spage>1</spage><epage>9</epage><pages>1-9</pages><issn>2314-6133</issn><eissn>2314-6141</eissn><abstract>Liver regeneration after partial hepatectomy (PH) is a highly orchestrated biological process in which synchronized hepatocyte proliferation is induced after massive liver mass loss. Hepatocyte proliferation could be regulated by multiple signals, such as miRNAs and autophagy, but underlying mechanism remains unclear. Here a functional miRNA during liver regeneration was identified and its underlying mechanism was delineated in vitro and in vivo. We found that miR-1907 was highly upregulated during liver regeneration after 2/3 PH at various timepoints. The level of miR-1907 was also increased in normal liver cell line treated with HGF at different concentrations. Functionally, miR-1907 enhanced hepatocyte proliferation in vitro and in vivo, and the liver/body weight ratio in miR-1907-overexpressed mice was significantly higher in comparison to the control mice after 2/3 PH. Forced expression of miR-1907 promoted autophagy activation of hepatocyte. Importantly, autophagy inhibition significantly attenuated miR-1907-induced hepatocyte proliferation and the liver/body weight ratio. Finally, GSK3β, a suppressor of autophagy signaling, was identified as the direct target gene of miR-1907. Taken together, miR-1907 accelerates hepatocyte proliferation during liver regeneration by activating autophagy; thus pharmacological intervention regulating miR-1907/autophagy axis may be therapeutically beneficial in liver transplantation and liver failure by inducing liver regeneration.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Publishing Corporation</pub><pmid>30151380</pmid><doi>10.1155/2018/3817057</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0002-2912-6016</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Activation Analysis Animals Apoptosis Autophagy Biological activity Body weight Cell Proliferation China Growth factors Hepatectomy Hepatocytes Hepatology Laboratories Liver Liver cancer Liver diseases Liver Regeneration Liver transplantation Mice Mice, Inbred C57BL MicroRNA MicroRNAs MicroRNAs - metabolism miRNA Mutation Phagocytosis Pharmacology Regeneration Target recognition Transplantation Transplantation of organs, tissues, etc Up-Regulation |
title | Partial Hepatectomy-Induced Upregulation of miR-1907 Accelerates Liver Regeneration by Activation Autophagy |
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