{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,25]],"date-time":"2026-07-25T22:04:23Z","timestamp":1785017063562,"version":"3.55.0"},"reference-count":30,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2009,1,20]],"date-time":"2009-01-20T00:00:00Z","timestamp":1232409600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Eur J Clin Investigation"],"published-print":{"date-parts":[[2009,2]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p><jats:bold>Background\u2002<\/jats:bold> Nidogen\u20102, an extracellular matrix protein, is ubiquitous in renal basement membranes linking the laminin and collagen IV networks. Nidogen\u20102\u2010deficient (nidogen\u20102<jats:sup>\u2212\/\u2013<\/jats:sup>) mice do not exhibit a phenotype, and renal basement membranes appear normal. The functional role of nidogen\u20102 in the adult kidney under pathological conditions however remains unclear. We tested the hypothesis that nidogen\u20102 mediated cell\u2010matrix interactions are important to maintain glomerular integrity and structure in renal hyperperfusion and hypertension.<\/jats:p><jats:p><jats:bold>Materials and methods\u2002<\/jats:bold> Two weeks after unilateral nephrectomy (UNX), desoxycorticosterone (DOCA)\u2010salt hypertension was induced in nidogen\u20102<jats:sup>\u2212\/\u2013<\/jats:sup> mice and their wild type littermates for 6\u00a0weeks. Renal damage was assessed by means of semiquantitative scoring, morphometric analysis, immunohistochemistry and measurement of serum creatinine and albumin excretion.<\/jats:p><jats:p><jats:bold>Results\u2002<\/jats:bold> UNX alone resulted in a very mild increase in renal damage in nidogen\u20102<jats:sup>\u2212\/\u2013<\/jats:sup> mice compared to wild type animals. Following DOCA\u2010salt treatment, blood pressure, serum creatinine and albumin excretion were significantly higher in nidogen\u20102<jats:sup>\u2212\/\u2013<\/jats:sup> than in wild type mice. In addition, nidogen\u20102<jats:sup>\u2212\/\u2013<\/jats:sup> mice showed increased mesangial cell hyperplasia and matrix expansion with higher expression of fibronectin and its receptor \u03b18 integrin. Glomerular capillaries were significantly reduced in size and number.<\/jats:p><jats:p><jats:bold>Conclusions\u2002<\/jats:bold> We demonstrate that in both mild and severe glomerular damage, lack of nidogen\u20102 is associated with: (i) increased mesangioproliferation; (ii) higher mesangial matrix expansion; and (iii) reduction in glomerular capillary supply. These findings suggest a critical role for nidogen\u20102 in the maintenance of glomerular structure in the diseased kidney.<\/jats:p>","DOI":"10.1111\/j.1365-2362.2008.02065.x","type":"journal-article","created":{"date-parts":[[2009,1,20]],"date-time":"2009-01-20T10:33:18Z","timestamp":1232447598000},"page":"116-125","source":"Crossref","is-referenced-by-count":13,"title":["Lack of nidogen\u20102 increases blood pressure, glomerular and tubulointerstitial damage in DOCA\u2010salt hypertension"],"prefix":"10.1111","volume":"39","author":[{"given":"K.","family":"Amann","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"C. S.","family":"Haas","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"G. 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