CaMK4 compromises podocyte function in autoimmune and nonautoimmune kidney disease
Podocyte malfunction occurs in autoimmune and nonautoimmune kidney disease. Calcium signaling is essential for podocyte injury, but the role of Ca2+/calmodulin-dependent kinase (CaMK) signaling in podocytes has not been fully explored. We report that podocytes from patients with lupus nephritis and...
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| Veröffentlicht in: | The Journal of clinical investigation 2018-08, Vol.128 (8), p.3445-3459 |
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| creator | Maeda, Kayaho Otomo, Kotaro Yoshida, Nobuya Abu-Asab, Mones S Ichinose, Kunihiro Nishino, Tomoya Kono, Michihito Ferretti, Andrew Bhargava, Rhea Maruyama, Shoichi Bickerton, Sean Fahmy, Tarek M Tsokos, Maria G Tsokos, George C |
| description | Podocyte malfunction occurs in autoimmune and nonautoimmune kidney disease. Calcium signaling is essential for podocyte injury, but the role of Ca2+/calmodulin-dependent kinase (CaMK) signaling in podocytes has not been fully explored. We report that podocytes from patients with lupus nephritis and focal segmental glomerulosclerosis and lupus-prone and lipopolysaccharide- or adriamycin-treated mice display increased expression of CaMK IV (CaMK4), but not CaMK2. Mechanistically, CaMK4 modulated podocyte motility by altering the expression of the GTPases Rac1 and RhoA and suppressed the expression of nephrin, synaptopodin, and actin fibers in podocytes. In addition, it phosphorylated the scaffold protein 14-3-3β, which resulted in the release and degradation of synaptopodin. Targeted delivery of a CaMK4 inhibitor to podocytes preserved their ultrastructure, averted immune complex deposition and crescent formation, and suppressed proteinuria in lupus-prone mice and proteinuria in mice exposed to lipopolysaccharide-induced podocyte injury by preserving nephrin/synaptopodin expression. In animals exposed to adriamycin, podocyte-specific delivery of a CaMK4 inhibitor prevented and reversed podocyte injury and renal disease. We conclude that CaMK4 is pivotal in immune and nonimmune podocyte injury and that its targeted cell-specific inhibition preserves podocyte structure and function and should have therapeutic value in lupus nephritis and podocytopathies, including focal segmental glomerulosclerosis. |
| doi_str_mv | 10.1172/JCI99507 |
| format | Article |
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Calcium signaling is essential for podocyte injury, but the role of Ca2+/calmodulin-dependent kinase (CaMK) signaling in podocytes has not been fully explored. We report that podocytes from patients with lupus nephritis and focal segmental glomerulosclerosis and lupus-prone and lipopolysaccharide- or adriamycin-treated mice display increased expression of CaMK IV (CaMK4), but not CaMK2. Mechanistically, CaMK4 modulated podocyte motility by altering the expression of the GTPases Rac1 and RhoA and suppressed the expression of nephrin, synaptopodin, and actin fibers in podocytes. In addition, it phosphorylated the scaffold protein 14-3-3β, which resulted in the release and degradation of synaptopodin. Targeted delivery of a CaMK4 inhibitor to podocytes preserved their ultrastructure, averted immune complex deposition and crescent formation, and suppressed proteinuria in lupus-prone mice and proteinuria in mice exposed to lipopolysaccharide-induced podocyte injury by preserving nephrin/synaptopodin expression. In animals exposed to adriamycin, podocyte-specific delivery of a CaMK4 inhibitor prevented and reversed podocyte injury and renal disease. We conclude that CaMK4 is pivotal in immune and nonimmune podocyte injury and that its targeted cell-specific inhibition preserves podocyte structure and function and should have therapeutic value in lupus nephritis and podocytopathies, including focal segmental glomerulosclerosis.</description><identifier>ISSN: 0021-9738</identifier><identifier>EISSN: 1558-8238</identifier><identifier>DOI: 10.1172/JCI99507</identifier><identifier>PMID: 29985166</identifier><language>eng</language><publisher>United States: American Society for Clinical Investigation</publisher><subject>Actin ; Analysis ; Autoimmune diseases ; Biomedical research ; Biopsy ; Ca2+/calmodulin-dependent protein kinase ; Calcium signalling ; Calcium-binding protein ; Calmodulin ; Care and treatment ; Development and progression ; GTPases ; Kidney diseases ; Kidneys ; Kinases ; Lipopolysaccharides ; Lupus ; Lupus nephritis ; Motility ; Nephritis ; Phosphorylation ; Proteins ; Proteinuria ; Rac1 protein ; RhoA protein ; Rodents ; Structure-function relationships ; Trends ; Ultrastructure</subject><ispartof>The Journal of clinical investigation, 2018-08, Vol.128 (8), p.3445-3459</ispartof><rights>COPYRIGHT 2018 American Society for Clinical Investigation</rights><rights>Copyright American Society for Clinical Investigation Aug 2018</rights><rights>Copyright © 2018, American Society for Clinical Investigation 2018 American Society for Clinical Investigation</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c643t-624250bad31e25e49010a676c64c8f5eae7adfd9d1b695031e4c1645e33d15d03</citedby><cites>FETCH-LOGICAL-c643t-624250bad31e25e49010a676c64c8f5eae7adfd9d1b695031e4c1645e33d15d03</cites><orcidid>0000-0001-8794-7106 ; 0000-0001-8740-4179 ; 0000-0001-9589-2360</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/PMC6063476/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6063476/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29985166$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Maeda, Kayaho</creatorcontrib><creatorcontrib>Otomo, Kotaro</creatorcontrib><creatorcontrib>Yoshida, Nobuya</creatorcontrib><creatorcontrib>Abu-Asab, Mones S</creatorcontrib><creatorcontrib>Ichinose, Kunihiro</creatorcontrib><creatorcontrib>Nishino, Tomoya</creatorcontrib><creatorcontrib>Kono, Michihito</creatorcontrib><creatorcontrib>Ferretti, Andrew</creatorcontrib><creatorcontrib>Bhargava, Rhea</creatorcontrib><creatorcontrib>Maruyama, Shoichi</creatorcontrib><creatorcontrib>Bickerton, Sean</creatorcontrib><creatorcontrib>Fahmy, Tarek M</creatorcontrib><creatorcontrib>Tsokos, Maria G</creatorcontrib><creatorcontrib>Tsokos, George C</creatorcontrib><title>CaMK4 compromises podocyte function in autoimmune and nonautoimmune kidney disease</title><title>The Journal of clinical investigation</title><addtitle>J Clin Invest</addtitle><description>Podocyte malfunction occurs in autoimmune and nonautoimmune kidney disease. Calcium signaling is essential for podocyte injury, but the role of Ca2+/calmodulin-dependent kinase (CaMK) signaling in podocytes has not been fully explored. We report that podocytes from patients with lupus nephritis and focal segmental glomerulosclerosis and lupus-prone and lipopolysaccharide- or adriamycin-treated mice display increased expression of CaMK IV (CaMK4), but not CaMK2. Mechanistically, CaMK4 modulated podocyte motility by altering the expression of the GTPases Rac1 and RhoA and suppressed the expression of nephrin, synaptopodin, and actin fibers in podocytes. In addition, it phosphorylated the scaffold protein 14-3-3β, which resulted in the release and degradation of synaptopodin. Targeted delivery of a CaMK4 inhibitor to podocytes preserved their ultrastructure, averted immune complex deposition and crescent formation, and suppressed proteinuria in lupus-prone mice and proteinuria in mice exposed to lipopolysaccharide-induced podocyte injury by preserving nephrin/synaptopodin expression. In animals exposed to adriamycin, podocyte-specific delivery of a CaMK4 inhibitor prevented and reversed podocyte injury and renal disease. We conclude that CaMK4 is pivotal in immune and nonimmune podocyte injury and that its targeted cell-specific inhibition preserves podocyte structure and function and should have therapeutic value in lupus nephritis and podocytopathies, including focal segmental glomerulosclerosis.</description><subject>Actin</subject><subject>Analysis</subject><subject>Autoimmune diseases</subject><subject>Biomedical research</subject><subject>Biopsy</subject><subject>Ca2+/calmodulin-dependent protein kinase</subject><subject>Calcium signalling</subject><subject>Calcium-binding protein</subject><subject>Calmodulin</subject><subject>Care and treatment</subject><subject>Development and progression</subject><subject>GTPases</subject><subject>Kidney diseases</subject><subject>Kidneys</subject><subject>Kinases</subject><subject>Lipopolysaccharides</subject><subject>Lupus</subject><subject>Lupus nephritis</subject><subject>Motility</subject><subject>Nephritis</subject><subject>Phosphorylation</subject><subject>Proteins</subject><subject>Proteinuria</subject><subject>Rac1 protein</subject><subject>RhoA protein</subject><subject>Rodents</subject><subject>Structure-function relationships</subject><subject>Trends</subject><subject>Ultrastructure</subject><issn>0021-9738</issn><issn>1558-8238</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqNktuKFDEQhoMo7rgKPoE0CKIXvSadQ3ffCMvgYXRlYT3chkxSPZO1Oxk7ybLz9mZwdpmWuZBcBKq--pOq-hF6TvAZIXX19vN80bYc1w_QjHDelE1Fm4dohnFFyramzQl6EsI1xoQxzh6jk6ptG06EmKGrufr6hRXaD5vRDzZAKDbeeL2NUHTJ6Wi9K6wrVIreDkNyUChnCufdQeSXNQ62hcnlKsBT9KhTfYBn-_sU_fjw_vv8U3lx-XExP78otWA0lqJiFcdLZSiBigNrMcFK1CJnddNxUFAr05nWkKXIvWWKaSIYB0oN4QbTU_Tur-4mLQcwGlwcVS83ox3UuJVeWTnNOLuWK38jBRaU1SILvN4LjP53ghBlHoCGvlcOfAqywqImtGG4zujLf9Brn0aX25MVwRxjIcQBtVI9SOs6n9_VO1F5zjkmoiWkyVR5hFqBg_xJ76CzOTzhz47w-RgYrD5a8GZSkJkIt3GlUghy8e3q_9nLn1P21QG7BtXHdfB92nkkTMH9YPXoQxihu18KwXJnWHln2Iy-OFziPXjnUPoHWMjhQw</recordid><startdate>20180801</startdate><enddate>20180801</enddate><creator>Maeda, 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compromises podocyte function in autoimmune and nonautoimmune kidney disease</title><author>Maeda, Kayaho ; Otomo, Kotaro ; Yoshida, Nobuya ; Abu-Asab, Mones S ; Ichinose, Kunihiro ; Nishino, Tomoya ; Kono, Michihito ; Ferretti, Andrew ; Bhargava, Rhea ; Maruyama, Shoichi ; Bickerton, Sean ; Fahmy, Tarek M ; Tsokos, Maria G ; Tsokos, George C</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c643t-624250bad31e25e49010a676c64c8f5eae7adfd9d1b695031e4c1645e33d15d03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Actin</topic><topic>Analysis</topic><topic>Autoimmune diseases</topic><topic>Biomedical research</topic><topic>Biopsy</topic><topic>Ca2+/calmodulin-dependent protein kinase</topic><topic>Calcium signalling</topic><topic>Calcium-binding protein</topic><topic>Calmodulin</topic><topic>Care and treatment</topic><topic>Development and progression</topic><topic>GTPases</topic><topic>Kidney diseases</topic><topic>Kidneys</topic><topic>Kinases</topic><topic>Lipopolysaccharides</topic><topic>Lupus</topic><topic>Lupus nephritis</topic><topic>Motility</topic><topic>Nephritis</topic><topic>Phosphorylation</topic><topic>Proteins</topic><topic>Proteinuria</topic><topic>Rac1 protein</topic><topic>RhoA protein</topic><topic>Rodents</topic><topic>Structure-function relationships</topic><topic>Trends</topic><topic>Ultrastructure</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Maeda, Kayaho</creatorcontrib><creatorcontrib>Otomo, Kotaro</creatorcontrib><creatorcontrib>Yoshida, Nobuya</creatorcontrib><creatorcontrib>Abu-Asab, Mones S</creatorcontrib><creatorcontrib>Ichinose, Kunihiro</creatorcontrib><creatorcontrib>Nishino, Tomoya</creatorcontrib><creatorcontrib>Kono, Michihito</creatorcontrib><creatorcontrib>Ferretti, Andrew</creatorcontrib><creatorcontrib>Bhargava, 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Andrew</au><au>Bhargava, Rhea</au><au>Maruyama, Shoichi</au><au>Bickerton, Sean</au><au>Fahmy, Tarek M</au><au>Tsokos, Maria G</au><au>Tsokos, George C</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CaMK4 compromises podocyte function in autoimmune and nonautoimmune kidney disease</atitle><jtitle>The Journal of clinical investigation</jtitle><addtitle>J Clin Invest</addtitle><date>2018-08-01</date><risdate>2018</risdate><volume>128</volume><issue>8</issue><spage>3445</spage><epage>3459</epage><pages>3445-3459</pages><issn>0021-9738</issn><eissn>1558-8238</eissn><abstract>Podocyte malfunction occurs in autoimmune and nonautoimmune kidney disease. Calcium signaling is essential for podocyte injury, but the role of Ca2+/calmodulin-dependent kinase (CaMK) signaling in podocytes has not been fully explored. We report that podocytes from patients with lupus nephritis and focal segmental glomerulosclerosis and lupus-prone and lipopolysaccharide- or adriamycin-treated mice display increased expression of CaMK IV (CaMK4), but not CaMK2. Mechanistically, CaMK4 modulated podocyte motility by altering the expression of the GTPases Rac1 and RhoA and suppressed the expression of nephrin, synaptopodin, and actin fibers in podocytes. In addition, it phosphorylated the scaffold protein 14-3-3β, which resulted in the release and degradation of synaptopodin. Targeted delivery of a CaMK4 inhibitor to podocytes preserved their ultrastructure, averted immune complex deposition and crescent formation, and suppressed proteinuria in lupus-prone mice and proteinuria in mice exposed to lipopolysaccharide-induced podocyte injury by preserving nephrin/synaptopodin expression. In animals exposed to adriamycin, podocyte-specific delivery of a CaMK4 inhibitor prevented and reversed podocyte injury and renal disease. We conclude that CaMK4 is pivotal in immune and nonimmune podocyte injury and that its targeted cell-specific inhibition preserves podocyte structure and function and should have therapeutic value in lupus nephritis and podocytopathies, including focal segmental glomerulosclerosis.</abstract><cop>United States</cop><pub>American Society for Clinical Investigation</pub><pmid>29985166</pmid><doi>10.1172/JCI99507</doi><tpages>15</tpages><orcidid>https://orcid.org/0000-0001-8794-7106</orcidid><orcidid>https://orcid.org/0000-0001-8740-4179</orcidid><orcidid>https://orcid.org/0000-0001-9589-2360</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | The Journal of clinical investigation, 2018-08, Vol.128 (8), p.3445-3459 |
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| source | Journals@Ovid Complete; EZB-FREE-00999 freely available EZB journals; PubMed Central; Alma/SFX Local Collection |
| subjects | Actin Analysis Autoimmune diseases Biomedical research Biopsy Ca2+/calmodulin-dependent protein kinase Calcium signalling Calcium-binding protein Calmodulin Care and treatment Development and progression GTPases Kidney diseases Kidneys Kinases Lipopolysaccharides Lupus Lupus nephritis Motility Nephritis Phosphorylation Proteins Proteinuria Rac1 protein RhoA protein Rodents Structure-function relationships Trends Ultrastructure |
| title | CaMK4 compromises podocyte function in autoimmune and nonautoimmune kidney disease |
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