ZFYVE21 promotes endothelial nitric oxide signaling and vascular barrier function in the kidney during aging
ZFYVE21 is an ancient, endosome-associated protein that is highly expressed in endothelial cells (ECs) but whose function(s) in vivo are undefined. Here, we identified ZFYVE21 as an essential regulator of vascular barrier function in the aging kidney. ZFYVE21 levels significantly decline in ECs in a...
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| Veröffentlicht in: | Kidney international 2024-09, Vol.106 (3), p.419-432 |
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| creator | Jiang, Quan Song, Guiyu He, Liying Li, Xue Jiang, Bo Wang, Qianxun Wang, Shaoxun Kim, Catherine Barkestani, Mahsa Nouri Lopez, Roberto Fan, Matthew Wanniarachchi, Kujani Quaranta, Maya Tian, Xuefei Mani, Arya Gonzalez, Anjelica Goodwin, Julie E. Sessa, William C. Ishibe, Shuta Jane-wit, Dan |
| description | ZFYVE21 is an ancient, endosome-associated protein that is highly expressed in endothelial cells (ECs) but whose function(s) in vivo are undefined. Here, we identified ZFYVE21 as an essential regulator of vascular barrier function in the aging kidney. ZFYVE21 levels significantly decline in ECs in aged human and mouse kidneys. To investigate attendant effects, we generated EC-specific Zfyve21-/- reporter mice. These knockout mice developed accelerated aging phenotypes including reduced endothelial nitric oxide (ENOS) activity, failure to thrive, and kidney insufficiency. Kidneys from Zfyve21 EC-/- mice showed interstitial edema and glomerular EC injury. ZFYVE21-mediated phenotypes were not programmed developmentally as loss of ZFYVE21 in ECs during adulthood phenocopied its loss prenatally, and a nitric oxide donor normalized kidney function in adult hosts. Using live cell imaging and human kidney organ cultures, we found that in a GTPase Rab5- and protein kinase Akt-dependent manner, ZFYVE21 reduced vesicular levels of inhibitory caveolin-1 and promoted transfer of Golgi-derived ENOS to a perinuclear Rab5+ vesicular population to functionally sustain ENOS activity. Thus, our work defines a ZFYVE21- mediated trafficking mechanism sustaining ENOS activity and demonstrates the relevance of this pathway for maintaining kidney function with aging.
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| doi_str_mv | 10.1016/j.kint.2024.05.007 |
| format | Article |
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[Display omitted]</description><identifier>ISSN: 0085-2538</identifier><identifier>ISSN: 1523-1755</identifier><identifier>EISSN: 1523-1755</identifier><identifier>DOI: 10.1016/j.kint.2024.05.007</identifier><identifier>PMID: 38797325</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>aging ; Aging - metabolism ; Aging - physiology ; Animals ; Caveolin 1 - genetics ; Caveolin 1 - metabolism ; endosomes ; endothelial cell dysfunction ; Endothelial Cells - metabolism ; ENOS ; Golgi Apparatus - metabolism ; Humans ; Kidney - metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Nitric Oxide - metabolism ; Nitric Oxide Donors - pharmacology ; Nitric Oxide Synthase Type III - genetics ; Nitric Oxide Synthase Type III - metabolism ; Phenotype ; Proto-Oncogene Proteins c-akt - metabolism ; rab5 GTP-Binding Proteins - genetics ; rab5 GTP-Binding Proteins - metabolism ; Renal Insufficiency - genetics ; Renal Insufficiency - metabolism ; Renal Insufficiency - physiopathology ; Signal Transduction</subject><ispartof>Kidney international, 2024-09, Vol.106 (3), p.419-432</ispartof><rights>2024 International Society of Nephrology</rights><rights>Copyright © 2024 International Society of Nephrology. Published by Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c281t-2d9af93a738b3fd95bfbb8fb054006c8978c296d81a45db8996dd7d9e1538a653</cites><orcidid>0000-0001-7115-0362</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38797325$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jiang, Quan</creatorcontrib><creatorcontrib>Song, Guiyu</creatorcontrib><creatorcontrib>He, Liying</creatorcontrib><creatorcontrib>Li, Xue</creatorcontrib><creatorcontrib>Jiang, Bo</creatorcontrib><creatorcontrib>Wang, Qianxun</creatorcontrib><creatorcontrib>Wang, Shaoxun</creatorcontrib><creatorcontrib>Kim, Catherine</creatorcontrib><creatorcontrib>Barkestani, Mahsa Nouri</creatorcontrib><creatorcontrib>Lopez, Roberto</creatorcontrib><creatorcontrib>Fan, Matthew</creatorcontrib><creatorcontrib>Wanniarachchi, Kujani</creatorcontrib><creatorcontrib>Quaranta, Maya</creatorcontrib><creatorcontrib>Tian, Xuefei</creatorcontrib><creatorcontrib>Mani, Arya</creatorcontrib><creatorcontrib>Gonzalez, Anjelica</creatorcontrib><creatorcontrib>Goodwin, Julie E.</creatorcontrib><creatorcontrib>Sessa, William C.</creatorcontrib><creatorcontrib>Ishibe, Shuta</creatorcontrib><creatorcontrib>Jane-wit, Dan</creatorcontrib><title>ZFYVE21 promotes endothelial nitric oxide signaling and vascular barrier function in the kidney during aging</title><title>Kidney international</title><addtitle>Kidney Int</addtitle><description>ZFYVE21 is an ancient, endosome-associated protein that is highly expressed in endothelial cells (ECs) but whose function(s) in vivo are undefined. Here, we identified ZFYVE21 as an essential regulator of vascular barrier function in the aging kidney. ZFYVE21 levels significantly decline in ECs in aged human and mouse kidneys. To investigate attendant effects, we generated EC-specific Zfyve21-/- reporter mice. These knockout mice developed accelerated aging phenotypes including reduced endothelial nitric oxide (ENOS) activity, failure to thrive, and kidney insufficiency. Kidneys from Zfyve21 EC-/- mice showed interstitial edema and glomerular EC injury. ZFYVE21-mediated phenotypes were not programmed developmentally as loss of ZFYVE21 in ECs during adulthood phenocopied its loss prenatally, and a nitric oxide donor normalized kidney function in adult hosts. Using live cell imaging and human kidney organ cultures, we found that in a GTPase Rab5- and protein kinase Akt-dependent manner, ZFYVE21 reduced vesicular levels of inhibitory caveolin-1 and promoted transfer of Golgi-derived ENOS to a perinuclear Rab5+ vesicular population to functionally sustain ENOS activity. Thus, our work defines a ZFYVE21- mediated trafficking mechanism sustaining ENOS activity and demonstrates the relevance of this pathway for maintaining kidney function with aging.
[Display omitted]</description><subject>aging</subject><subject>Aging - metabolism</subject><subject>Aging - physiology</subject><subject>Animals</subject><subject>Caveolin 1 - genetics</subject><subject>Caveolin 1 - metabolism</subject><subject>endosomes</subject><subject>endothelial cell dysfunction</subject><subject>Endothelial Cells - metabolism</subject><subject>ENOS</subject><subject>Golgi Apparatus - metabolism</subject><subject>Humans</subject><subject>Kidney - metabolism</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Nitric Oxide - metabolism</subject><subject>Nitric Oxide Donors - pharmacology</subject><subject>Nitric Oxide Synthase Type III - genetics</subject><subject>Nitric Oxide Synthase Type III - metabolism</subject><subject>Phenotype</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>rab5 GTP-Binding Proteins - genetics</subject><subject>rab5 GTP-Binding Proteins - metabolism</subject><subject>Renal Insufficiency - genetics</subject><subject>Renal Insufficiency - metabolism</subject><subject>Renal Insufficiency - physiopathology</subject><subject>Signal Transduction</subject><issn>0085-2538</issn><issn>1523-1755</issn><issn>1523-1755</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kM1O3DAUhS1EVabAC7BAXrJJem2PE1tig9BAKyF101ZqN5Zj3wweMg7YCYK3r6dDWXZzf6RzjnQ-Qs4Y1AxY83lTP4Q41Rz4sgZZA7QHZMEkFxVrpTwkCwAlKy6FOiKfct5A-bWAj-RIqFa3gssFGX7f_Pq54ow-pnE7TpgpRj9O9zgEO9AYphQcHV-CR5rDOtohxDW10dNnm9082EQ7m1LARPs5uimMkYZIi58-BB_xlfo5_bWsyzwhH3o7ZDx928fkx83q-_WX6u7b7dfrq7vKccWminttey1sK1Qneq9l13ed6juQS4DGKd0qx3XjFbNL6Tuly-1br5GVqraR4phc7HNLqacZ82S2ITscBhtxnLMR0EArWbOEIuV7qUtjzgl785jC1qZXw8DsKJuN2VE2O8oGpCmUi-n8LX_utujfLf-wFsHlXoCl5XOhY7ILGB36kNBNxo_hf_l_AB3mj0k</recordid><startdate>202409</startdate><enddate>202409</enddate><creator>Jiang, Quan</creator><creator>Song, Guiyu</creator><creator>He, Liying</creator><creator>Li, Xue</creator><creator>Jiang, Bo</creator><creator>Wang, Qianxun</creator><creator>Wang, Shaoxun</creator><creator>Kim, Catherine</creator><creator>Barkestani, Mahsa Nouri</creator><creator>Lopez, Roberto</creator><creator>Fan, Matthew</creator><creator>Wanniarachchi, Kujani</creator><creator>Quaranta, Maya</creator><creator>Tian, Xuefei</creator><creator>Mani, Arya</creator><creator>Gonzalez, Anjelica</creator><creator>Goodwin, Julie E.</creator><creator>Sessa, William C.</creator><creator>Ishibe, Shuta</creator><creator>Jane-wit, Dan</creator><general>Elsevier Inc</general><scope>6I.</scope><scope>AAFTH</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>7X8</scope><orcidid>https://orcid.org/0000-0001-7115-0362</orcidid></search><sort><creationdate>202409</creationdate><title>ZFYVE21 promotes endothelial nitric oxide signaling and vascular barrier function in the kidney during aging</title><author>Jiang, Quan ; Song, Guiyu ; He, Liying ; Li, Xue ; Jiang, Bo ; Wang, Qianxun ; Wang, Shaoxun ; Kim, Catherine ; Barkestani, Mahsa Nouri ; Lopez, Roberto ; Fan, Matthew ; Wanniarachchi, Kujani ; Quaranta, Maya ; Tian, Xuefei ; Mani, Arya ; Gonzalez, Anjelica ; Goodwin, Julie E. ; Sessa, William C. ; Ishibe, Shuta ; Jane-wit, Dan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c281t-2d9af93a738b3fd95bfbb8fb054006c8978c296d81a45db8996dd7d9e1538a653</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>aging</topic><topic>Aging - metabolism</topic><topic>Aging - physiology</topic><topic>Animals</topic><topic>Caveolin 1 - genetics</topic><topic>Caveolin 1 - metabolism</topic><topic>endosomes</topic><topic>endothelial cell dysfunction</topic><topic>Endothelial Cells - metabolism</topic><topic>ENOS</topic><topic>Golgi Apparatus - metabolism</topic><topic>Humans</topic><topic>Kidney - metabolism</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Nitric Oxide - metabolism</topic><topic>Nitric Oxide Donors - pharmacology</topic><topic>Nitric Oxide Synthase Type III - genetics</topic><topic>Nitric Oxide Synthase Type III - metabolism</topic><topic>Phenotype</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>rab5 GTP-Binding Proteins - genetics</topic><topic>rab5 GTP-Binding Proteins - metabolism</topic><topic>Renal Insufficiency - genetics</topic><topic>Renal Insufficiency - metabolism</topic><topic>Renal Insufficiency - physiopathology</topic><topic>Signal Transduction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jiang, Quan</creatorcontrib><creatorcontrib>Song, Guiyu</creatorcontrib><creatorcontrib>He, Liying</creatorcontrib><creatorcontrib>Li, Xue</creatorcontrib><creatorcontrib>Jiang, Bo</creatorcontrib><creatorcontrib>Wang, Qianxun</creatorcontrib><creatorcontrib>Wang, Shaoxun</creatorcontrib><creatorcontrib>Kim, Catherine</creatorcontrib><creatorcontrib>Barkestani, Mahsa Nouri</creatorcontrib><creatorcontrib>Lopez, Roberto</creatorcontrib><creatorcontrib>Fan, Matthew</creatorcontrib><creatorcontrib>Wanniarachchi, Kujani</creatorcontrib><creatorcontrib>Quaranta, Maya</creatorcontrib><creatorcontrib>Tian, Xuefei</creatorcontrib><creatorcontrib>Mani, Arya</creatorcontrib><creatorcontrib>Gonzalez, Anjelica</creatorcontrib><creatorcontrib>Goodwin, Julie E.</creatorcontrib><creatorcontrib>Sessa, William C.</creatorcontrib><creatorcontrib>Ishibe, Shuta</creatorcontrib><creatorcontrib>Jane-wit, Dan</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Kidney international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jiang, Quan</au><au>Song, Guiyu</au><au>He, Liying</au><au>Li, Xue</au><au>Jiang, Bo</au><au>Wang, Qianxun</au><au>Wang, Shaoxun</au><au>Kim, Catherine</au><au>Barkestani, Mahsa Nouri</au><au>Lopez, Roberto</au><au>Fan, Matthew</au><au>Wanniarachchi, Kujani</au><au>Quaranta, Maya</au><au>Tian, Xuefei</au><au>Mani, Arya</au><au>Gonzalez, Anjelica</au><au>Goodwin, Julie E.</au><au>Sessa, William C.</au><au>Ishibe, Shuta</au><au>Jane-wit, Dan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>ZFYVE21 promotes endothelial nitric oxide signaling and vascular barrier function in the kidney during aging</atitle><jtitle>Kidney international</jtitle><addtitle>Kidney Int</addtitle><date>2024-09</date><risdate>2024</risdate><volume>106</volume><issue>3</issue><spage>419</spage><epage>432</epage><pages>419-432</pages><issn>0085-2538</issn><issn>1523-1755</issn><eissn>1523-1755</eissn><abstract>ZFYVE21 is an ancient, endosome-associated protein that is highly expressed in endothelial cells (ECs) but whose function(s) in vivo are undefined. Here, we identified ZFYVE21 as an essential regulator of vascular barrier function in the aging kidney. ZFYVE21 levels significantly decline in ECs in aged human and mouse kidneys. To investigate attendant effects, we generated EC-specific Zfyve21-/- reporter mice. These knockout mice developed accelerated aging phenotypes including reduced endothelial nitric oxide (ENOS) activity, failure to thrive, and kidney insufficiency. Kidneys from Zfyve21 EC-/- mice showed interstitial edema and glomerular EC injury. ZFYVE21-mediated phenotypes were not programmed developmentally as loss of ZFYVE21 in ECs during adulthood phenocopied its loss prenatally, and a nitric oxide donor normalized kidney function in adult hosts. Using live cell imaging and human kidney organ cultures, we found that in a GTPase Rab5- and protein kinase Akt-dependent manner, ZFYVE21 reduced vesicular levels of inhibitory caveolin-1 and promoted transfer of Golgi-derived ENOS to a perinuclear Rab5+ vesicular population to functionally sustain ENOS activity. Thus, our work defines a ZFYVE21- mediated trafficking mechanism sustaining ENOS activity and demonstrates the relevance of this pathway for maintaining kidney function with aging.
[Display omitted]</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>38797325</pmid><doi>10.1016/j.kint.2024.05.007</doi><tpages>14</tpages><orcidid>https://orcid.org/0000-0001-7115-0362</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | aging Aging - metabolism Aging - physiology Animals Caveolin 1 - genetics Caveolin 1 - metabolism endosomes endothelial cell dysfunction Endothelial Cells - metabolism ENOS Golgi Apparatus - metabolism Humans Kidney - metabolism Male Mice Mice, Inbred C57BL Mice, Knockout Nitric Oxide - metabolism Nitric Oxide Donors - pharmacology Nitric Oxide Synthase Type III - genetics Nitric Oxide Synthase Type III - metabolism Phenotype Proto-Oncogene Proteins c-akt - metabolism rab5 GTP-Binding Proteins - genetics rab5 GTP-Binding Proteins - metabolism Renal Insufficiency - genetics Renal Insufficiency - metabolism Renal Insufficiency - physiopathology Signal Transduction |
| title | ZFYVE21 promotes endothelial nitric oxide signaling and vascular barrier function in the kidney during aging |
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