Sorting Nexin 9 facilitates podocin endocytosis in the injured podocyte
The irreversibility of glomerulosclerotic changes depends on the degree of podocyte injury. We have previously demonstrated the endocytic translocation of podocin to the subcellular area in severely injured podocytes and found that this process is the primary disease trigger. Here we identified the...
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| Veröffentlicht in: | Scientific reports 2017-03, Vol.7 (1), p.43921-43921, Article 43921 |
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| creator | Sasaki, Yu Hidaka, Teruo Ueno, Takashi Akiba-Takagi, Miyuki Oliva Trejo, Juan Alejandro Seki, Takuto Nagai-Hosoe, Yoshiko Tanaka, Eriko Horikoshi, Satoshi Tomino, Yasuhiko Suzuki, Yusuke Asanuma, Katsuhiko |
| description | The irreversibility of glomerulosclerotic changes depends on the degree of podocyte injury. We have previously demonstrated the endocytic translocation of podocin to the subcellular area in severely injured podocytes and found that this process is the primary disease trigger. Here we identified the protein sorting nexin 9 (SNX9) as a novel facilitator of podocin endocytosis in a yeast two-hybrid analysis. SNX9 is involved in clathrin-mediated endocytosis, actin rearrangement and vesicle transport regulation. Our results revealed and confirmed that SNX9 interacts with podocin exclusively through the Bin–Amphiphysin–Rvs (BAR) domain of SNX9. Immunofluorescence staining revealed the expression of SNX9 in response to podocyte adriamycin-induced injury both
in vitro
and
in vivo
. Finally, an analysis of human glomerular disease biopsy samples demonstrated strong SNX9 expression and co-localization with podocin in samples representative of severe podocyte injury, such as IgA nephropathy with poor prognosis, membranous nephropathy and focal segmental glomerulosclerosis. In conclusion, we identified SNX9 as a facilitator of podocin endocytosis in severe podocyte injury and demonstrated the expression of SNX9 in the podocytes of both nephropathy model mice and human patients with irreversible glomerular disease. |
| doi_str_mv | 10.1038/srep43921 |
| format | Article |
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in vitro
and
in vivo
. Finally, an analysis of human glomerular disease biopsy samples demonstrated strong SNX9 expression and co-localization with podocin in samples representative of severe podocyte injury, such as IgA nephropathy with poor prognosis, membranous nephropathy and focal segmental glomerulosclerosis. In conclusion, we identified SNX9 as a facilitator of podocin endocytosis in severe podocyte injury and demonstrated the expression of SNX9 in the podocytes of both nephropathy model mice and human patients with irreversible glomerular disease.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/srep43921</identifier><identifier>PMID: 28266622</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/109 ; 13/51 ; 14/19 ; 38/109 ; 38/111 ; 38/89 ; 631/45/612/1237 ; 631/80/313/1461 ; 64/60 ; 692/4022/1585/2759 ; 692/4022/272/1684/1587/2101 ; 82/29 ; 82/80 ; Actin ; Animals ; Biopsy ; Clathrin ; Disease Models, Animal ; Endocytosis ; Glomerulonephritis, IGA - pathology ; Glomerulonephritis, Membranous - pathology ; Glomerulosclerosis, Focal Segmental - pathology ; Humanities and Social Sciences ; Humans ; IgA nephropathy ; Immunofluorescence ; Immunoglobulin A ; Immunohistochemistry ; Intracellular Signaling Peptides and Proteins - metabolism ; Localization ; Membrane Proteins - metabolism ; Membranous nephropathy ; Mice, Inbred BALB C ; multidisciplinary ; Nexin ; Podocytes - metabolism ; Protein Binding ; Protein Interaction Mapping ; Protein transport ; Rodents ; Science ; Sorting Nexins - metabolism ; Translocation ; Two-Hybrid System Techniques ; Yeasts</subject><ispartof>Scientific reports, 2017-03, Vol.7 (1), p.43921-43921, Article 43921</ispartof><rights>The Author(s) 2017</rights><rights>Copyright Nature Publishing Group Mar 2017</rights><rights>Copyright © 2017, The Author(s) 2017 The Author(s)</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c504t-4b141b37a8a6ae66ff2a09ac8a76d6e8ce62cdb1538249080f731d02553c0c733</citedby><cites>FETCH-LOGICAL-c504t-4b141b37a8a6ae66ff2a09ac8a76d6e8ce62cdb1538249080f731d02553c0c733</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5339724/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5339724/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,729,782,786,866,887,27931,27932,41127,42196,51583,53798,53800</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28266622$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sasaki, Yu</creatorcontrib><creatorcontrib>Hidaka, Teruo</creatorcontrib><creatorcontrib>Ueno, Takashi</creatorcontrib><creatorcontrib>Akiba-Takagi, Miyuki</creatorcontrib><creatorcontrib>Oliva Trejo, Juan Alejandro</creatorcontrib><creatorcontrib>Seki, Takuto</creatorcontrib><creatorcontrib>Nagai-Hosoe, Yoshiko</creatorcontrib><creatorcontrib>Tanaka, Eriko</creatorcontrib><creatorcontrib>Horikoshi, Satoshi</creatorcontrib><creatorcontrib>Tomino, Yasuhiko</creatorcontrib><creatorcontrib>Suzuki, Yusuke</creatorcontrib><creatorcontrib>Asanuma, Katsuhiko</creatorcontrib><title>Sorting Nexin 9 facilitates podocin endocytosis in the injured podocyte</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><addtitle>Sci Rep</addtitle><description>The irreversibility of glomerulosclerotic changes depends on the degree of podocyte injury. We have previously demonstrated the endocytic translocation of podocin to the subcellular area in severely injured podocytes and found that this process is the primary disease trigger. Here we identified the protein sorting nexin 9 (SNX9) as a novel facilitator of podocin endocytosis in a yeast two-hybrid analysis. SNX9 is involved in clathrin-mediated endocytosis, actin rearrangement and vesicle transport regulation. Our results revealed and confirmed that SNX9 interacts with podocin exclusively through the Bin–Amphiphysin–Rvs (BAR) domain of SNX9. Immunofluorescence staining revealed the expression of SNX9 in response to podocyte adriamycin-induced injury both
in vitro
and
in vivo
. Finally, an analysis of human glomerular disease biopsy samples demonstrated strong SNX9 expression and co-localization with podocin in samples representative of severe podocyte injury, such as IgA nephropathy with poor prognosis, membranous nephropathy and focal segmental glomerulosclerosis. In conclusion, we identified SNX9 as a facilitator of podocin endocytosis in severe podocyte injury and demonstrated the expression of SNX9 in the podocytes of both nephropathy model mice and human patients with irreversible glomerular disease.</description><subject>13/109</subject><subject>13/51</subject><subject>14/19</subject><subject>38/109</subject><subject>38/111</subject><subject>38/89</subject><subject>631/45/612/1237</subject><subject>631/80/313/1461</subject><subject>64/60</subject><subject>692/4022/1585/2759</subject><subject>692/4022/272/1684/1587/2101</subject><subject>82/29</subject><subject>82/80</subject><subject>Actin</subject><subject>Animals</subject><subject>Biopsy</subject><subject>Clathrin</subject><subject>Disease Models, Animal</subject><subject>Endocytosis</subject><subject>Glomerulonephritis, IGA - pathology</subject><subject>Glomerulonephritis, Membranous - pathology</subject><subject>Glomerulosclerosis, Focal Segmental - pathology</subject><subject>Humanities and Social Sciences</subject><subject>Humans</subject><subject>IgA nephropathy</subject><subject>Immunofluorescence</subject><subject>Immunoglobulin A</subject><subject>Immunohistochemistry</subject><subject>Intracellular Signaling Peptides and Proteins - metabolism</subject><subject>Localization</subject><subject>Membrane Proteins - metabolism</subject><subject>Membranous nephropathy</subject><subject>Mice, Inbred BALB C</subject><subject>multidisciplinary</subject><subject>Nexin</subject><subject>Podocytes - metabolism</subject><subject>Protein Binding</subject><subject>Protein Interaction Mapping</subject><subject>Protein transport</subject><subject>Rodents</subject><subject>Science</subject><subject>Sorting Nexins - metabolism</subject><subject>Translocation</subject><subject>Two-Hybrid System Techniques</subject><subject>Yeasts</subject><issn>2045-2322</issn><issn>2045-2322</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>C6C</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>eNplkU9rGzEQxUVoiI3jQ75AWMilDTjV_5UuhRCatBDSQ5uzkLWztsx65UjaUn_7KtgxTqvLk2Z-PM3wELog-IZgpj6nCBvONCUnaEwxFzPKKP1wdB-haUorXI6gmhN9hkZUUSklpWP08DPE7PtF9QR_fF_pqrXOdz7bDKnahCa4UoW-6DaH5FNVnnkJRVZDhGaHbDOco9PWdgmme52g5_uvv-6-zR5_PHy_u32cOYF5nvE54WTOaqustCBl21KLtXXK1rKRoBxI6po5EUxRrrHCbc1Ig6kQzGFXMzZBX3a-m2G-hsZBn6PtzCb6tY1bE6w37zu9X5pF-G0EY7qmvBh83BvE8DJAymbtk4Ousz2EIRmiakE4V0wU9OofdBWG2Jf1DNGYMckx1YX6tKNcDKmE0R6GIdi8JmQOCRX28nj6A_mWRwGud0AqrX4B8ejL_9z-Av01mj8</recordid><startdate>20170307</startdate><enddate>20170307</enddate><creator>Sasaki, Yu</creator><creator>Hidaka, Teruo</creator><creator>Ueno, Takashi</creator><creator>Akiba-Takagi, Miyuki</creator><creator>Oliva Trejo, Juan Alejandro</creator><creator>Seki, Takuto</creator><creator>Nagai-Hosoe, Yoshiko</creator><creator>Tanaka, Eriko</creator><creator>Horikoshi, Satoshi</creator><creator>Tomino, Yasuhiko</creator><creator>Suzuki, Yusuke</creator><creator>Asanuma, Katsuhiko</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>C6C</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>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</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>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>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20170307</creationdate><title>Sorting Nexin 9 facilitates podocin endocytosis in the injured podocyte</title><author>Sasaki, Yu ; Hidaka, Teruo ; Ueno, Takashi ; Akiba-Takagi, Miyuki ; Oliva Trejo, Juan Alejandro ; Seki, Takuto ; Nagai-Hosoe, Yoshiko ; Tanaka, Eriko ; Horikoshi, Satoshi ; Tomino, Yasuhiko ; Suzuki, Yusuke ; Asanuma, Katsuhiko</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c504t-4b141b37a8a6ae66ff2a09ac8a76d6e8ce62cdb1538249080f731d02553c0c733</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>13/109</topic><topic>13/51</topic><topic>14/19</topic><topic>38/109</topic><topic>38/111</topic><topic>38/89</topic><topic>631/45/612/1237</topic><topic>631/80/313/1461</topic><topic>64/60</topic><topic>692/4022/1585/2759</topic><topic>692/4022/272/1684/1587/2101</topic><topic>82/29</topic><topic>82/80</topic><topic>Actin</topic><topic>Animals</topic><topic>Biopsy</topic><topic>Clathrin</topic><topic>Disease Models, Animal</topic><topic>Endocytosis</topic><topic>Glomerulonephritis, IGA - pathology</topic><topic>Glomerulonephritis, Membranous - pathology</topic><topic>Glomerulosclerosis, Focal Segmental - pathology</topic><topic>Humanities and Social Sciences</topic><topic>Humans</topic><topic>IgA nephropathy</topic><topic>Immunofluorescence</topic><topic>Immunoglobulin A</topic><topic>Immunohistochemistry</topic><topic>Intracellular Signaling Peptides and Proteins - metabolism</topic><topic>Localization</topic><topic>Membrane Proteins - metabolism</topic><topic>Membranous nephropathy</topic><topic>Mice, Inbred BALB C</topic><topic>multidisciplinary</topic><topic>Nexin</topic><topic>Podocytes - metabolism</topic><topic>Protein Binding</topic><topic>Protein Interaction Mapping</topic><topic>Protein transport</topic><topic>Rodents</topic><topic>Science</topic><topic>Sorting Nexins - metabolism</topic><topic>Translocation</topic><topic>Two-Hybrid System Techniques</topic><topic>Yeasts</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sasaki, Yu</creatorcontrib><creatorcontrib>Hidaka, Teruo</creatorcontrib><creatorcontrib>Ueno, Takashi</creatorcontrib><creatorcontrib>Akiba-Takagi, Miyuki</creatorcontrib><creatorcontrib>Oliva Trejo, Juan Alejandro</creatorcontrib><creatorcontrib>Seki, Takuto</creatorcontrib><creatorcontrib>Nagai-Hosoe, Yoshiko</creatorcontrib><creatorcontrib>Tanaka, Eriko</creatorcontrib><creatorcontrib>Horikoshi, Satoshi</creatorcontrib><creatorcontrib>Tomino, Yasuhiko</creatorcontrib><creatorcontrib>Suzuki, Yusuke</creatorcontrib><creatorcontrib>Asanuma, Katsuhiko</creatorcontrib><collection>Springer Nature OA Free Journals</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>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>Science Database (Alumni Edition)</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>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>Access via ProQuest (Open Access)</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 Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Scientific reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sasaki, Yu</au><au>Hidaka, Teruo</au><au>Ueno, Takashi</au><au>Akiba-Takagi, Miyuki</au><au>Oliva Trejo, Juan Alejandro</au><au>Seki, Takuto</au><au>Nagai-Hosoe, Yoshiko</au><au>Tanaka, Eriko</au><au>Horikoshi, Satoshi</au><au>Tomino, Yasuhiko</au><au>Suzuki, Yusuke</au><au>Asanuma, Katsuhiko</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Sorting Nexin 9 facilitates podocin endocytosis in the injured podocyte</atitle><jtitle>Scientific reports</jtitle><stitle>Sci Rep</stitle><addtitle>Sci Rep</addtitle><date>2017-03-07</date><risdate>2017</risdate><volume>7</volume><issue>1</issue><spage>43921</spage><epage>43921</epage><pages>43921-43921</pages><artnum>43921</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>The irreversibility of glomerulosclerotic changes depends on the degree of podocyte injury. We have previously demonstrated the endocytic translocation of podocin to the subcellular area in severely injured podocytes and found that this process is the primary disease trigger. Here we identified the protein sorting nexin 9 (SNX9) as a novel facilitator of podocin endocytosis in a yeast two-hybrid analysis. SNX9 is involved in clathrin-mediated endocytosis, actin rearrangement and vesicle transport regulation. Our results revealed and confirmed that SNX9 interacts with podocin exclusively through the Bin–Amphiphysin–Rvs (BAR) domain of SNX9. Immunofluorescence staining revealed the expression of SNX9 in response to podocyte adriamycin-induced injury both
in vitro
and
in vivo
. Finally, an analysis of human glomerular disease biopsy samples demonstrated strong SNX9 expression and co-localization with podocin in samples representative of severe podocyte injury, such as IgA nephropathy with poor prognosis, membranous nephropathy and focal segmental glomerulosclerosis. In conclusion, we identified SNX9 as a facilitator of podocin endocytosis in severe podocyte injury and demonstrated the expression of SNX9 in the podocytes of both nephropathy model mice and human patients with irreversible glomerular disease.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>28266622</pmid><doi>10.1038/srep43921</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 13/109 13/51 14/19 38/109 38/111 38/89 631/45/612/1237 631/80/313/1461 64/60 692/4022/1585/2759 692/4022/272/1684/1587/2101 82/29 82/80 Actin Animals Biopsy Clathrin Disease Models, Animal Endocytosis Glomerulonephritis, IGA - pathology Glomerulonephritis, Membranous - pathology Glomerulosclerosis, Focal Segmental - pathology Humanities and Social Sciences Humans IgA nephropathy Immunofluorescence Immunoglobulin A Immunohistochemistry Intracellular Signaling Peptides and Proteins - metabolism Localization Membrane Proteins - metabolism Membranous nephropathy Mice, Inbred BALB C multidisciplinary Nexin Podocytes - metabolism Protein Binding Protein Interaction Mapping Protein transport Rodents Science Sorting Nexins - metabolism Translocation Two-Hybrid System Techniques Yeasts |
| title | Sorting Nexin 9 facilitates podocin endocytosis in the injured podocyte |
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