Disruption of Myosin 1e Promotes Podocyte Injury
Myosin 1e (Myo1e) is one of two Src homology 3 domain-containing "long-tailed" type I myosins in vertebrates, whose functions in health and disease are incompletely understood. Here, we demonstrate that Myo1e localizes to podocytes in the kidney. We generated Myo1e-knockout mice and found...
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| Veröffentlicht in: | Journal of the American Society of Nephrology 2009, Vol.20 (1), p.86-94 |
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| container_title | Journal of the American Society of Nephrology |
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| creator | KRENDEL, Mira KIM, Sangwon V WILLINGER, Tim TONG WANG KASHGARIAN, Michael FLAVELL, Richard A MOOSEKER, Mark S |
| description | Myosin 1e (Myo1e) is one of two Src homology 3 domain-containing "long-tailed" type I myosins in vertebrates, whose functions in health and disease are incompletely understood. Here, we demonstrate that Myo1e localizes to podocytes in the kidney. We generated Myo1e-knockout mice and found that they exhibit proteinuria, signs of chronic renal injury, and kidney inflammation. At the ultrastructural level, renal tissue from Myo1e-null mice demonstrates changes characteristic of glomerular disease, including a thickened and disorganized glomerular basement membrane and flattened podocyte foot processes. These observations suggest that Myo1e plays an important role in podocyte function and normal glomerular filtration. |
| doi_str_mv | 10.1681/asn.2007111172 |
| format | Article |
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Here, we demonstrate that Myo1e localizes to podocytes in the kidney. We generated Myo1e-knockout mice and found that they exhibit proteinuria, signs of chronic renal injury, and kidney inflammation. At the ultrastructural level, renal tissue from Myo1e-null mice demonstrates changes characteristic of glomerular disease, including a thickened and disorganized glomerular basement membrane and flattened podocyte foot processes. These observations suggest that Myo1e plays an important role in podocyte function and normal glomerular filtration.</description><identifier>ISSN: 1046-6673</identifier><identifier>EISSN: 1533-3450</identifier><identifier>DOI: 10.1681/asn.2007111172</identifier><identifier>PMID: 19005011</identifier><identifier>CODEN: JASNEU</identifier><language>eng</language><publisher>Washington, DC: American Society of Nephrology</publisher><subject>Animals ; Basic Research ; Biological and medical sciences ; Blood Urea Nitrogen ; Glomerular Filtration Rate ; Kidney Diseases - etiology ; Kidney Glomerulus - pathology ; Medical sciences ; Mice ; Mice, Knockout ; Myosins - analysis ; Myosins - physiology ; Nephrology. Urinary tract diseases ; Podocytes - chemistry ; Podocytes - pathology</subject><ispartof>Journal of the American Society of Nephrology, 2009, Vol.20 (1), p.86-94</ispartof><rights>2009 INIST-CNRS</rights><rights>Copyright © 2009 by the American Society of Nephrology</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c529t-7edc8c125d4150a82df28e1574b6596282abdc42f8398f5e78ac36b2c25d79073</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2615733/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2615733/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,4009,27902,27903,27904,53769,53771</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=21036733$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19005011$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>KRENDEL, Mira</creatorcontrib><creatorcontrib>KIM, Sangwon V</creatorcontrib><creatorcontrib>WILLINGER, Tim</creatorcontrib><creatorcontrib>TONG WANG</creatorcontrib><creatorcontrib>KASHGARIAN, Michael</creatorcontrib><creatorcontrib>FLAVELL, Richard A</creatorcontrib><creatorcontrib>MOOSEKER, Mark S</creatorcontrib><title>Disruption of Myosin 1e Promotes Podocyte Injury</title><title>Journal of the American Society of Nephrology</title><addtitle>J Am Soc Nephrol</addtitle><description>Myosin 1e (Myo1e) is one of two Src homology 3 domain-containing "long-tailed" type I myosins in vertebrates, whose functions in health and disease are incompletely understood. Here, we demonstrate that Myo1e localizes to podocytes in the kidney. We generated Myo1e-knockout mice and found that they exhibit proteinuria, signs of chronic renal injury, and kidney inflammation. At the ultrastructural level, renal tissue from Myo1e-null mice demonstrates changes characteristic of glomerular disease, including a thickened and disorganized glomerular basement membrane and flattened podocyte foot processes. These observations suggest that Myo1e plays an important role in podocyte function and normal glomerular filtration.</description><subject>Animals</subject><subject>Basic Research</subject><subject>Biological and medical sciences</subject><subject>Blood Urea Nitrogen</subject><subject>Glomerular Filtration Rate</subject><subject>Kidney Diseases - etiology</subject><subject>Kidney Glomerulus - pathology</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Myosins - analysis</subject><subject>Myosins - physiology</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Podocytes - chemistry</subject><subject>Podocytes - pathology</subject><issn>1046-6673</issn><issn>1533-3450</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkElPwzAQhS0EoqVw5YhygVuKl3jJBakqWyWWSsDZchwHUiVxsROk_HtcNWphLjPSfPPe6AFwjuAUMYGulW-mGEKOQnF8AMaIEhKThMLDMMOExYxxMgIn3q8gRBRzfgxGKIWQQoTGAN6W3nXrtrRNZIvoube-bCJkoqWztW2Nj5Y2t7pvTbRoVp3rT8FRoSpvzoY-AR_3d-_zx_jp9WExnz3FmuK0jbnJtdAI0zxBFCqB8wILgyhPMkZThgVWWa4TXAiSioIaLpQmLMM6XPAUcjIBN1vddZfVQcw0rVOVXLuyVq6XVpXy_6Ypv-Sn_ZGYBRdCgsDVIODsd2d8K-vSa1NVqjG28zLkkgrERQCnW1A7670zxc4EQbkJWc7eXuQ-5HBw8fe1PT6kGoDLAVBeq6pwqtGl33EYQcI2L_4C5zaELg</recordid><startdate>2009</startdate><enddate>2009</enddate><creator>KRENDEL, Mira</creator><creator>KIM, Sangwon V</creator><creator>WILLINGER, Tim</creator><creator>TONG WANG</creator><creator>KASHGARIAN, Michael</creator><creator>FLAVELL, Richard A</creator><creator>MOOSEKER, Mark S</creator><general>American Society of Nephrology</general><scope>IQODW</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><scope>5PM</scope></search><sort><creationdate>2009</creationdate><title>Disruption of Myosin 1e Promotes Podocyte Injury</title><author>KRENDEL, Mira ; KIM, Sangwon V ; WILLINGER, Tim ; TONG WANG ; KASHGARIAN, Michael ; FLAVELL, Richard A ; MOOSEKER, Mark S</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c529t-7edc8c125d4150a82df28e1574b6596282abdc42f8398f5e78ac36b2c25d79073</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Animals</topic><topic>Basic Research</topic><topic>Biological and medical sciences</topic><topic>Blood Urea Nitrogen</topic><topic>Glomerular Filtration Rate</topic><topic>Kidney Diseases - etiology</topic><topic>Kidney Glomerulus - pathology</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Myosins - analysis</topic><topic>Myosins - physiology</topic><topic>Nephrology. Urinary tract diseases</topic><topic>Podocytes - chemistry</topic><topic>Podocytes - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>KRENDEL, Mira</creatorcontrib><creatorcontrib>KIM, Sangwon V</creatorcontrib><creatorcontrib>WILLINGER, Tim</creatorcontrib><creatorcontrib>TONG WANG</creatorcontrib><creatorcontrib>KASHGARIAN, Michael</creatorcontrib><creatorcontrib>FLAVELL, Richard A</creatorcontrib><creatorcontrib>MOOSEKER, Mark S</creatorcontrib><collection>Pascal-Francis</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><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of the American Society of Nephrology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>KRENDEL, Mira</au><au>KIM, Sangwon V</au><au>WILLINGER, Tim</au><au>TONG WANG</au><au>KASHGARIAN, Michael</au><au>FLAVELL, Richard A</au><au>MOOSEKER, Mark S</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Disruption of Myosin 1e Promotes Podocyte Injury</atitle><jtitle>Journal of the American Society of Nephrology</jtitle><addtitle>J Am Soc Nephrol</addtitle><date>2009</date><risdate>2009</risdate><volume>20</volume><issue>1</issue><spage>86</spage><epage>94</epage><pages>86-94</pages><issn>1046-6673</issn><eissn>1533-3450</eissn><coden>JASNEU</coden><abstract>Myosin 1e (Myo1e) is one of two Src homology 3 domain-containing "long-tailed" type I myosins in vertebrates, whose functions in health and disease are incompletely understood. 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| subjects | Animals Basic Research Biological and medical sciences Blood Urea Nitrogen Glomerular Filtration Rate Kidney Diseases - etiology Kidney Glomerulus - pathology Medical sciences Mice Mice, Knockout Myosins - analysis Myosins - physiology Nephrology. Urinary tract diseases Podocytes - chemistry Podocytes - pathology |
| title | Disruption of Myosin 1e Promotes Podocyte Injury |
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