Generation of mice with hepatocyte-specific conditional deletion of sphingosine kinase 1
SphK1 gene has different roles in various types of cells in liver diseases, but most studies are based on global knockout mice, which hampers the study on the cellular and molecular mechanisms of SphK1. In order to further study the role of SphK1 in liver, SphK1 conditional knockout mice were constr...
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Veröffentlicht in: | Transgenic research 2020-08, Vol.29 (4), p.419-428 |
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description | SphK1 gene has different roles in various types of cells in liver diseases, but most studies are based on global knockout mice, which hampers the study on the cellular and molecular mechanisms of SphK1. In order to further study the role of SphK1 in liver, SphK1 conditional knockout mice were constructed. A liver-specific SphK1 gene knockout mouse model was constructed by the Cre/Loxp recombinant enzyme system. PCR technologies and western blotting were used to identified the elimination of SphK1 gene in hepatocytes. SphK1
flox/flox
mice were used as a control group to verify the effectiveness of SphK1 liver-specific knockout mice from the profile, pathology, and serology of mice. The ablation of SphK1 in hepatic parenchymal cells was demonstrated by fluorescent in situ hybridization and the contents of S1P and Sph were measured by ELISA kit. The genotypes of liver in SphK1 conditional knockout mice were different from that of other organs. The mRNA and protein levels of SphK1 in liver tissue of SphK1 conditional knockout mice were almost depleted by compared with SphK1
flox/flox
mice. Physiology and pathology showed no significant difference between SphK1 liver conditional knockout mice and SphK1
flox/flox
mice. Additionally, SphK1 was eliminated in hepatocytes, leading to the reduce of S1P content in hepatocytes and liver tissues and the increase of Sph content in hepatocytes. The model of SphK1 gene liver conditional knockout mice was successfully constructed, providing a tool for the study of the roles of SphK1 in hepatocyte and liver diseases. |
doi_str_mv | 10.1007/s11248-020-00211-0 |
format | Article |
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flox/flox
mice were used as a control group to verify the effectiveness of SphK1 liver-specific knockout mice from the profile, pathology, and serology of mice. The ablation of SphK1 in hepatic parenchymal cells was demonstrated by fluorescent in situ hybridization and the contents of S1P and Sph were measured by ELISA kit. The genotypes of liver in SphK1 conditional knockout mice were different from that of other organs. The mRNA and protein levels of SphK1 in liver tissue of SphK1 conditional knockout mice were almost depleted by compared with SphK1
flox/flox
mice. Physiology and pathology showed no significant difference between SphK1 liver conditional knockout mice and SphK1
flox/flox
mice. Additionally, SphK1 was eliminated in hepatocytes, leading to the reduce of S1P content in hepatocytes and liver tissues and the increase of Sph content in hepatocytes. The model of SphK1 gene liver conditional knockout mice was successfully constructed, providing a tool for the study of the roles of SphK1 in hepatocyte and liver diseases.</description><identifier>ISSN: 0962-8819</identifier><identifier>EISSN: 1573-9368</identifier><identifier>DOI: 10.1007/s11248-020-00211-0</identifier><language>eng</language><publisher>Cham: Springer International Publishing</publisher><subject>Animal Genetics and Genomics ; Biomedical and Life Sciences ; Biomedical Engineering/Biotechnology ; Enzyme-linked immunosorbent assay ; Fluorescence in situ hybridization ; Gene deletion ; Genetic Engineering ; Genotypes ; Hepatocytes ; Kinases ; Life Sciences ; Liver diseases ; Molecular Medicine ; Molecular modelling ; mRNA ; Original Paper ; Plant Genetics and Genomics ; Rodents ; Serology ; Sphingosine kinase ; Transgenics ; Western blotting</subject><ispartof>Transgenic research, 2020-08, Vol.29 (4), p.419-428</ispartof><rights>Springer Nature Switzerland AG 2020</rights><rights>Springer Nature Switzerland AG 2020.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c352t-806d7d27135b20db95d5fbfc32117b200b971a7cbf1abb1743499644facd29563</citedby><cites>FETCH-LOGICAL-c352t-806d7d27135b20db95d5fbfc32117b200b971a7cbf1abb1743499644facd29563</cites><orcidid>0000-0002-5783-6883</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11248-020-00211-0$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11248-020-00211-0$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids></links><search><creatorcontrib>Yu, Jinfeng</creatorcontrib><creatorcontrib>Dong, Jiale</creatorcontrib><creatorcontrib>Chen, Kangdi</creatorcontrib><creatorcontrib>Ding, Yaping</creatorcontrib><creatorcontrib>Yang, Zhicheng</creatorcontrib><creatorcontrib>Lan, Tian</creatorcontrib><title>Generation of mice with hepatocyte-specific conditional deletion of sphingosine kinase 1</title><title>Transgenic research</title><addtitle>Transgenic Res</addtitle><description>SphK1 gene has different roles in various types of cells in liver diseases, but most studies are based on global knockout mice, which hampers the study on the cellular and molecular mechanisms of SphK1. In order to further study the role of SphK1 in liver, SphK1 conditional knockout mice were constructed. A liver-specific SphK1 gene knockout mouse model was constructed by the Cre/Loxp recombinant enzyme system. PCR technologies and western blotting were used to identified the elimination of SphK1 gene in hepatocytes. SphK1
flox/flox
mice were used as a control group to verify the effectiveness of SphK1 liver-specific knockout mice from the profile, pathology, and serology of mice. The ablation of SphK1 in hepatic parenchymal cells was demonstrated by fluorescent in situ hybridization and the contents of S1P and Sph were measured by ELISA kit. The genotypes of liver in SphK1 conditional knockout mice were different from that of other organs. The mRNA and protein levels of SphK1 in liver tissue of SphK1 conditional knockout mice were almost depleted by compared with SphK1
flox/flox
mice. Physiology and pathology showed no significant difference between SphK1 liver conditional knockout mice and SphK1
flox/flox
mice. Additionally, SphK1 was eliminated in hepatocytes, leading to the reduce of S1P content in hepatocytes and liver tissues and the increase of Sph content in hepatocytes. The model of SphK1 gene liver conditional knockout mice was successfully constructed, providing a tool for the study of the roles of SphK1 in hepatocyte and liver diseases.</description><subject>Animal Genetics and Genomics</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedical Engineering/Biotechnology</subject><subject>Enzyme-linked immunosorbent assay</subject><subject>Fluorescence in situ hybridization</subject><subject>Gene deletion</subject><subject>Genetic Engineering</subject><subject>Genotypes</subject><subject>Hepatocytes</subject><subject>Kinases</subject><subject>Life Sciences</subject><subject>Liver diseases</subject><subject>Molecular Medicine</subject><subject>Molecular modelling</subject><subject>mRNA</subject><subject>Original Paper</subject><subject>Plant Genetics and Genomics</subject><subject>Rodents</subject><subject>Serology</subject><subject>Sphingosine kinase</subject><subject>Transgenics</subject><subject>Western blotting</subject><issn>0962-8819</issn><issn>1573-9368</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</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><recordid>eNp9kMFKAzEURYMoWKs_4Crgxk30JZmZJEspWoWCGwV3IZPJtKnTZJxMEf_e1CqCC1cPHudcuBehcwpXFEBcJ0pZIQkwIACMUgIHaEJLwYnilTxEE1AVI1JSdYxOUloDZE3yCXqZu-AGM_oYcGzxxluH3_24wivXmzHaj9GR1DvrW2-xjaHxO9R0uHGd-7FSv_JhGZMPDr_6YJLD9BQdtaZL7uz7TtHz3e3T7J4sHucPs5sFsbxkI5FQNaJhgvKyZtDUqmzKtm4tzyVE_kCtBDXC1i01dU1FwQulqqJojW2YKis-RZf73H6Ib1uXRr3xybquM8HFbdKsYFXWlJAZvfiDruN2yGV2FGeVLDnwTLE9ZYeY0uBa3Q9-Y4YPTUHvxtb7sXUeW3-NrSFLfC-lDIelG36j_7E-AaPHgXE</recordid><startdate>20200801</startdate><enddate>20200801</enddate><creator>Yu, Jinfeng</creator><creator>Dong, Jiale</creator><creator>Chen, Kangdi</creator><creator>Ding, Yaping</creator><creator>Yang, Zhicheng</creator><creator>Lan, Tian</creator><general>Springer International Publishing</general><general>Springer Nature B.V</general><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7TK</scope><scope>7TM</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</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>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>RC3</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-5783-6883</orcidid></search><sort><creationdate>20200801</creationdate><title>Generation of mice with hepatocyte-specific conditional deletion of sphingosine kinase 1</title><author>Yu, Jinfeng ; Dong, Jiale ; Chen, Kangdi ; Ding, Yaping ; Yang, Zhicheng ; Lan, Tian</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c352t-806d7d27135b20db95d5fbfc32117b200b971a7cbf1abb1743499644facd29563</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Animal Genetics and Genomics</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedical Engineering/Biotechnology</topic><topic>Enzyme-linked immunosorbent assay</topic><topic>Fluorescence in situ hybridization</topic><topic>Gene deletion</topic><topic>Genetic Engineering</topic><topic>Genotypes</topic><topic>Hepatocytes</topic><topic>Kinases</topic><topic>Life Sciences</topic><topic>Liver diseases</topic><topic>Molecular Medicine</topic><topic>Molecular modelling</topic><topic>mRNA</topic><topic>Original Paper</topic><topic>Plant Genetics and Genomics</topic><topic>Rodents</topic><topic>Serology</topic><topic>Sphingosine kinase</topic><topic>Transgenics</topic><topic>Western blotting</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yu, Jinfeng</creatorcontrib><creatorcontrib>Dong, Jiale</creatorcontrib><creatorcontrib>Chen, Kangdi</creatorcontrib><creatorcontrib>Ding, Yaping</creatorcontrib><creatorcontrib>Yang, Zhicheng</creatorcontrib><creatorcontrib>Lan, Tian</creatorcontrib><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical 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>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</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>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Transgenic research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yu, Jinfeng</au><au>Dong, Jiale</au><au>Chen, Kangdi</au><au>Ding, Yaping</au><au>Yang, Zhicheng</au><au>Lan, Tian</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Generation of mice with hepatocyte-specific conditional deletion of sphingosine kinase 1</atitle><jtitle>Transgenic research</jtitle><stitle>Transgenic Res</stitle><date>2020-08-01</date><risdate>2020</risdate><volume>29</volume><issue>4</issue><spage>419</spage><epage>428</epage><pages>419-428</pages><issn>0962-8819</issn><eissn>1573-9368</eissn><abstract>SphK1 gene has different roles in various types of cells in liver diseases, but most studies are based on global knockout mice, which hampers the study on the cellular and molecular mechanisms of SphK1. In order to further study the role of SphK1 in liver, SphK1 conditional knockout mice were constructed. A liver-specific SphK1 gene knockout mouse model was constructed by the Cre/Loxp recombinant enzyme system. PCR technologies and western blotting were used to identified the elimination of SphK1 gene in hepatocytes. SphK1
flox/flox
mice were used as a control group to verify the effectiveness of SphK1 liver-specific knockout mice from the profile, pathology, and serology of mice. The ablation of SphK1 in hepatic parenchymal cells was demonstrated by fluorescent in situ hybridization and the contents of S1P and Sph were measured by ELISA kit. The genotypes of liver in SphK1 conditional knockout mice were different from that of other organs. The mRNA and protein levels of SphK1 in liver tissue of SphK1 conditional knockout mice were almost depleted by compared with SphK1
flox/flox
mice. Physiology and pathology showed no significant difference between SphK1 liver conditional knockout mice and SphK1
flox/flox
mice. Additionally, SphK1 was eliminated in hepatocytes, leading to the reduce of S1P content in hepatocytes and liver tissues and the increase of Sph content in hepatocytes. The model of SphK1 gene liver conditional knockout mice was successfully constructed, providing a tool for the study of the roles of SphK1 in hepatocyte and liver diseases.</abstract><cop>Cham</cop><pub>Springer International Publishing</pub><doi>10.1007/s11248-020-00211-0</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0002-5783-6883</orcidid></addata></record> |
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subjects | Animal Genetics and Genomics Biomedical and Life Sciences Biomedical Engineering/Biotechnology Enzyme-linked immunosorbent assay Fluorescence in situ hybridization Gene deletion Genetic Engineering Genotypes Hepatocytes Kinases Life Sciences Liver diseases Molecular Medicine Molecular modelling mRNA Original Paper Plant Genetics and Genomics Rodents Serology Sphingosine kinase Transgenics Western blotting |
title | Generation of mice with hepatocyte-specific conditional deletion of sphingosine kinase 1 |
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