Myo1e impairment results in actin reorganization, podocyte dysfunction, and proteinuria in zebrafish and cultured podocytes
Podocytes serve as an important constituent of the glomerular filtration barrier. Recently, we and others identified Myo1e as a key molecular component of the podocyte cytoskeleton. Myo1e mRNA and protein was expressed in human and mouse kidney sections as determined by Northern blot and reverse tra...
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| Veröffentlicht in: | PloS one 2013-08, Vol.8 (8), p.e72750-e72750 |
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| creator | Mao, Jianhua Wang, Dayan Mataleena, Parikka He, Bing Niu, Dadi Katayama, Kan Xu, Xiangjun Ojala, Juha Rm Wang, Wenjing Shu, Qiang Du, Lizhong Liu, Aimin Pikkarainen, Timo Patrakka, Jaakko Tryggvason, Karl |
| description | Podocytes serve as an important constituent of the glomerular filtration barrier. Recently, we and others identified Myo1e as a key molecular component of the podocyte cytoskeleton.
Myo1e mRNA and protein was expressed in human and mouse kidney sections as determined by Northern blot and reverse transcriptase PCR, and its expression was more evident in podocytes by immunofluorescence. By specific knock-down of MYO1E in zebrafish, the injected larvae exhibited pericardial edema and pronephric cysts, consistent with the appearance of protein in condensed incubation supernate. Furthermore, specific inhibition of Myo1e expression in a conditionally immortalized podocyte cell line induced morphological changes, actin cytoskeleton rearrangement, and dysfunction in cell proliferation, migration, endocytosis, and adhesion with the glomerular basement membrane.
Our results revealed that Myo1e is a key component contributing to the functional integrity of podocytes. Its impairment may cause actin cytoskeleton re-organization, alteration of cell shape, and membrane transport, and podocyte drop-out from the glomerular basement membrane, which might eventually lead to an impaired glomerular filtration barrier and proteinuria. |
| doi_str_mv | 10.1371/journal.pone.0072750 |
| format | Article |
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Myo1e mRNA and protein was expressed in human and mouse kidney sections as determined by Northern blot and reverse transcriptase PCR, and its expression was more evident in podocytes by immunofluorescence. By specific knock-down of MYO1E in zebrafish, the injected larvae exhibited pericardial edema and pronephric cysts, consistent with the appearance of protein in condensed incubation supernate. Furthermore, specific inhibition of Myo1e expression in a conditionally immortalized podocyte cell line induced morphological changes, actin cytoskeleton rearrangement, and dysfunction in cell proliferation, migration, endocytosis, and adhesion with the glomerular basement membrane.
Our results revealed that Myo1e is a key component contributing to the functional integrity of podocytes. Its impairment may cause actin cytoskeleton re-organization, alteration of cell shape, and membrane transport, and podocyte drop-out from the glomerular basement membrane, which might eventually lead to an impaired glomerular filtration barrier and proteinuria.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0072750</identifier><identifier>PMID: 23977349</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Actin ; Actins - metabolism ; Animals ; Biochemistry ; Biology ; Biophysics ; Cell Count ; Cell migration ; Cell Migration Assays ; Cell Proliferation ; Cell Shape ; Cell size ; Cells, Cultured ; Cysts ; Cytoskeleton ; Cytoskeleton - metabolism ; Danio rerio ; DNA polymerases ; Down-Regulation ; Edema ; Endocytosis ; Fertilization ; Filtration ; Fluorescein-5-isothiocyanate - metabolism ; Gene Knockdown Techniques ; Hospitals ; Humans ; Immunofluorescence ; Impairment ; Kidney Diseases - metabolism ; Kidney Diseases - pathology ; Kidney Glomerulus - metabolism ; Kidneys ; Kinases ; Larvae ; Medicine ; Mice ; Muscle proteins ; Myosin Type I - metabolism ; Myosins - metabolism ; Nephrology ; Podocytes - metabolism ; Proteins ; Proteinuria ; Proteinuria - metabolism ; RNA ; RNA-directed DNA polymerase ; Rodents ; Transferrin - metabolism ; Zebrafish ; Zebrafish - metabolism ; Zebrafish Proteins - metabolism</subject><ispartof>PloS one, 2013-08, Vol.8 (8), p.e72750-e72750</ispartof><rights>COPYRIGHT 2013 Public Library of Science</rights><rights>2013 Mao et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2013 Mao et al 2013 Mao et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c730t-4ee9e87a55fb823dcfdbbbb409789dbceed2168e68c93d0d8840ee420c4b1c03</citedby><cites>FETCH-LOGICAL-c730t-4ee9e87a55fb823dcfdbbbb409789dbceed2168e68c93d0d8840ee420c4b1c03</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/PMC3747079/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3747079/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,551,724,777,781,861,882,2096,2915,23847,27905,27906,53772,53774,79349,79350</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23977349$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttp://kipublications.ki.se/Default.aspx?queryparsed=id:127295495$$DView record from Swedish Publication Index$$Hfree_for_read</backlink></links><search><contributor>Rastaldi, Maria Pia</contributor><creatorcontrib>Mao, Jianhua</creatorcontrib><creatorcontrib>Wang, Dayan</creatorcontrib><creatorcontrib>Mataleena, Parikka</creatorcontrib><creatorcontrib>He, Bing</creatorcontrib><creatorcontrib>Niu, Dadi</creatorcontrib><creatorcontrib>Katayama, Kan</creatorcontrib><creatorcontrib>Xu, Xiangjun</creatorcontrib><creatorcontrib>Ojala, Juha Rm</creatorcontrib><creatorcontrib>Wang, Wenjing</creatorcontrib><creatorcontrib>Shu, Qiang</creatorcontrib><creatorcontrib>Du, Lizhong</creatorcontrib><creatorcontrib>Liu, Aimin</creatorcontrib><creatorcontrib>Pikkarainen, Timo</creatorcontrib><creatorcontrib>Patrakka, Jaakko</creatorcontrib><creatorcontrib>Tryggvason, Karl</creatorcontrib><title>Myo1e impairment results in actin reorganization, podocyte dysfunction, and proteinuria in zebrafish and cultured podocytes</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Podocytes serve as an important constituent of the glomerular filtration barrier. Recently, we and others identified Myo1e as a key molecular component of the podocyte cytoskeleton.
Myo1e mRNA and protein was expressed in human and mouse kidney sections as determined by Northern blot and reverse transcriptase PCR, and its expression was more evident in podocytes by immunofluorescence. By specific knock-down of MYO1E in zebrafish, the injected larvae exhibited pericardial edema and pronephric cysts, consistent with the appearance of protein in condensed incubation supernate. Furthermore, specific inhibition of Myo1e expression in a conditionally immortalized podocyte cell line induced morphological changes, actin cytoskeleton rearrangement, and dysfunction in cell proliferation, migration, endocytosis, and adhesion with the glomerular basement membrane.
Our results revealed that Myo1e is a key component contributing to the functional integrity of podocytes. Its impairment may cause actin cytoskeleton re-organization, alteration of cell shape, and membrane transport, and podocyte drop-out from the glomerular basement membrane, which might eventually lead to an impaired glomerular filtration barrier and proteinuria.</description><subject>Actin</subject><subject>Actins - metabolism</subject><subject>Animals</subject><subject>Biochemistry</subject><subject>Biology</subject><subject>Biophysics</subject><subject>Cell Count</subject><subject>Cell migration</subject><subject>Cell Migration Assays</subject><subject>Cell Proliferation</subject><subject>Cell Shape</subject><subject>Cell size</subject><subject>Cells, Cultured</subject><subject>Cysts</subject><subject>Cytoskeleton</subject><subject>Cytoskeleton - metabolism</subject><subject>Danio rerio</subject><subject>DNA 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Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Mao, Jianhua</au><au>Wang, Dayan</au><au>Mataleena, Parikka</au><au>He, Bing</au><au>Niu, Dadi</au><au>Katayama, Kan</au><au>Xu, Xiangjun</au><au>Ojala, Juha Rm</au><au>Wang, Wenjing</au><au>Shu, Qiang</au><au>Du, Lizhong</au><au>Liu, Aimin</au><au>Pikkarainen, Timo</au><au>Patrakka, Jaakko</au><au>Tryggvason, Karl</au><au>Rastaldi, Maria Pia</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Myo1e impairment results in actin reorganization, podocyte dysfunction, and proteinuria in zebrafish and cultured podocytes</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2013-08-19</date><risdate>2013</risdate><volume>8</volume><issue>8</issue><spage>e72750</spage><epage>e72750</epage><pages>e72750-e72750</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Podocytes serve as an important constituent of the glomerular filtration barrier. Recently, we and others identified Myo1e as a key molecular component of the podocyte cytoskeleton.
Myo1e mRNA and protein was expressed in human and mouse kidney sections as determined by Northern blot and reverse transcriptase PCR, and its expression was more evident in podocytes by immunofluorescence. By specific knock-down of MYO1E in zebrafish, the injected larvae exhibited pericardial edema and pronephric cysts, consistent with the appearance of protein in condensed incubation supernate. Furthermore, specific inhibition of Myo1e expression in a conditionally immortalized podocyte cell line induced morphological changes, actin cytoskeleton rearrangement, and dysfunction in cell proliferation, migration, endocytosis, and adhesion with the glomerular basement membrane.
Our results revealed that Myo1e is a key component contributing to the functional integrity of podocytes. Its impairment may cause actin cytoskeleton re-organization, alteration of cell shape, and membrane transport, and podocyte drop-out from the glomerular basement membrane, which might eventually lead to an impaired glomerular filtration barrier and proteinuria.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>23977349</pmid><doi>10.1371/journal.pone.0072750</doi><tpages>e72750</tpages><oa>free_for_read</oa></addata></record> |
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| recordid | cdi_plos_journals_1430785906 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; SWEPUB Freely available online; Public Library of Science (PLoS); PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Actin Actins - metabolism Animals Biochemistry Biology Biophysics Cell Count Cell migration Cell Migration Assays Cell Proliferation Cell Shape Cell size Cells, Cultured Cysts Cytoskeleton Cytoskeleton - metabolism Danio rerio DNA polymerases Down-Regulation Edema Endocytosis Fertilization Filtration Fluorescein-5-isothiocyanate - metabolism Gene Knockdown Techniques Hospitals Humans Immunofluorescence Impairment Kidney Diseases - metabolism Kidney Diseases - pathology Kidney Glomerulus - metabolism Kidneys Kinases Larvae Medicine Mice Muscle proteins Myosin Type I - metabolism Myosins - metabolism Nephrology Podocytes - metabolism Proteins Proteinuria Proteinuria - metabolism RNA RNA-directed DNA polymerase Rodents Transferrin - metabolism Zebrafish Zebrafish - metabolism Zebrafish Proteins - metabolism |
| title | Myo1e impairment results in actin reorganization, podocyte dysfunction, and proteinuria in zebrafish and cultured podocytes |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-20T01%3A28%3A20IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Myo1e%20impairment%20results%20in%20actin%20reorganization,%20podocyte%20dysfunction,%20and%20proteinuria%20in%20zebrafish%20and%20cultured%20podocytes&rft.jtitle=PloS%20one&rft.au=Mao,%20Jianhua&rft.date=2013-08-19&rft.volume=8&rft.issue=8&rft.spage=e72750&rft.epage=e72750&rft.pages=e72750-e72750&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0072750&rft_dat=%3Cgale_plos_%3EA478215018%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1430785906&rft_id=info:pmid/23977349&rft_galeid=A478215018&rft_doaj_id=oai_doaj_org_article_2c9a35a44c984305adc2a89912cd188a&rfr_iscdi=true |