{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,22]],"date-time":"2026-10-22T12:00:27Z","timestamp":1792670427588,"version":"4.5.0"},"reference-count":61,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2012,7,26]],"date-time":"2012-07-26T00:00:00Z","timestamp":1343260800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["pathsocjournals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The Journal of Pathology"],"published-print":{"date-parts":[[2012,12]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Glomerular crescents are most common in rapidly progressive glomerulonephritis but also occur in non\u2010inflammatory chronic glomerulopathies; thus, factors other than inflammation should trigger crescent formation, eg vascular damage and plasma leakage. Here we report that Alport nephropathy in\n                    <jats:italic>Col4A3<\/jats:italic>\n                    \u2010deficient Sv129 mice is complicated by diffuse and global crescent formation in which proliferating parietal epithelial cells are the predominant cell type. Laminin staining and transmission and acellular scanning electron microscopy of acellular glomeruli documented disruptions and progressive disintegration of the glomerular basement membrane in\n                    <jats:italic>Col4A3<\/jats:italic>\n                    \u2010deficient mice. FITC\u2010dextran perfusion further revealed vascular leakage from glomerular capillaries into Bowman's space, further documented by fibrin deposits in the segmental crescents. Its pathogenic role was validated by showing that the fibrinolytic activity of recombinant urokinase partially prevented crescent formation. In addition,\n                    <jats:italic>in vitro<\/jats:italic>\n                    studies confirmed an additional mitogenic potential of serum on murine and human parietal epithelial cells. Furthermore, loss of parietal cell polarity and unpolarized secretion of extracellular matrix components were evident within fibrocellular crescents. Among 665 human Alport nephropathy biopsies, crescent formation was noted in 0.4%. We conclude that glomerular vascular injury and GBM breaks cause plasma leakage which triggers a wound healing programme involving the proliferation of parietal cells and their loss of polarity. This process can trigger cellular and fibrocellular crescent formation even in the absence of cellular inflammation and rupture of the Bowman's capsule. Copyright \u00a9 2012 Pathological Society of Great Britain and Ireland. Published by John Wiley &amp; Sons, Ltd.\n                  <\/jats:p>","DOI":"10.1002\/path.4046","type":"journal-article","created":{"date-parts":[[2012,5,3]],"date-time":"2012-05-03T05:13:56Z","timestamp":1336022036000},"page":"482-494","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":66,"title":["Plasma leakage through glomerular basement membrane ruptures triggers the proliferation of parietal epithelial cells and crescent formation in non\u2010inflammatory glomerular injury"],"prefix":"10.1002","volume":"228","author":[{"given":"Mi","family":"Ryu","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Adriana","family":"Migliorini","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nicolai","family":"Miosge","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Oliver","family":"Gross","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stuart","family":"Shankland","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paul T","family":"Brinkkoetter","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Henning","family":"Hagmann","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paola","family":"Romagnani","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Helen","family":"Liapis","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hans\u2010Joachim","family":"Anders","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2012,7,26]]},"reference":[{"key":"e_1_2_7_2_1","doi-asserted-by":"publisher","DOI":"10.1159\/000180578"},{"key":"e_1_2_7_3_1","volume-title":"Immunologic Renal Diseases","author":"Tipping PG","year":"2001"},{"key":"e_1_2_7_4_1","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.V7112271"},{"key":"e_1_2_7_5_1","doi-asserted-by":"publisher","DOI":"10.1097\/MNH.0b013e32834583ec"},{"key":"e_1_2_7_6_1","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.V11122381"},{"key":"e_1_2_7_7_1","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2009010122"},{"key":"e_1_2_7_8_1","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000102468.37809.C6"},{"key":"e_1_2_7_9_1","doi-asserted-by":"publisher","DOI":"10.1038\/nm1460"},{"key":"e_1_2_7_10_1","doi-asserted-by":"publisher","DOI":"10.1002\/stem.492"},{"key":"e_1_2_7_11_1","doi-asserted-by":"publisher","DOI":"10.1038\/nm.2550"},{"key":"e_1_2_7_12_1","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2007080926"},{"key":"e_1_2_7_13_1","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.00428.2009"},{"key":"e_1_2_7_14_1","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2010.472"},{"key":"e_1_2_7_15_1","doi-asserted-by":"publisher","DOI":"10.1038\/nature07039"},{"key":"e_1_2_7_16_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.tcb.2005.09.002"},{"key":"e_1_2_7_17_1","doi-asserted-by":"publisher","DOI":"10.1097\/01.ASN.0000098685.43700.28"},{"key":"e_1_2_7_18_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.humpath.2009.08.024"},{"key":"e_1_2_7_19_1","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2010.373"},{"key":"e_1_2_7_20_1","doi-asserted-by":"publisher","DOI":"10.1002\/path.2505"},{"key":"e_1_2_7_21_1","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2004100871"},{"key":"e_1_2_7_22_1","doi-asserted-by":"publisher","DOI":"10.1038\/sj.ki.5001521"},{"key":"e_1_2_7_23_1","doi-asserted-by":"publisher","DOI":"10.1002\/path.2979"},{"key":"e_1_2_7_24_1","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2003.00779.x"},{"key":"e_1_2_7_25_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2005.00423.x"},{"key":"e_1_2_7_26_1","doi-asserted-by":"publisher","DOI":"10.2353\/ajpath.2007.060937"},{"key":"e_1_2_7_27_1","first-page":"1591","article-title":"Organization of the myotendinous junction is dependent on the presence of alpha7beta1 integrin","volume":"79","author":"Miosge N","year":"1999","journal-title":"Lab Invest"},{"key":"e_1_2_7_28_1","first-page":"357","article-title":"Glomerular basement membrane discontinuities. 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