{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,17]],"date-time":"2026-02-17T15:13:13Z","timestamp":1771341193159,"version":"3.50.1"},"reference-count":34,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2008,12,2]],"date-time":"2008-12-02T00:00:00Z","timestamp":1228176000000},"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":[[2009,5]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Lack of the \u03b13 or \u03b14 chain of type IV collagen (COL4) causes autosomal recessive Alport nephropathy in humans and mice that is characterized by progressive glomerulosclerosis and tubulointerstitial disease. Renal pathology is associated with chemokine\u2010mediated macrophage infiltrates but their contribution to the progression of Alport nephropathy is unclear. We found Ccl2 to be expressed in increasing amounts during the progression of nephropathy in <jats:italic>Col4a3<\/jats:italic>\u2010deficient mice; hence, we blocked Ccl2 with anti\u2010Ccl2 Spiegelmers, biostable <jats:sc>L<\/jats:sc>\u2010enantiomeric RNA aptamers suitable for <jats:italic>in vivo<\/jats:italic> applications. Ccl2 blockade reduced the recruitment of <jats:italic>ex vivo<\/jats:italic>\u2010labelled macrophages into kidneys of <jats:italic>Col4a3<\/jats:italic>\u2010deficient mice. We therefore hypothesized that a prolonged course of Ccl2 blockade would reduce renal macrophage counts and prevent renal pathology in <jats:italic>Col4a3<\/jats:italic>\u2010deficient mice. Groups of <jats:italic>Col4a3<\/jats:italic>\u2010deficient mice received subcutaneous injections of either an anti\u2010mCcl2 Spiegelmer or non\u2010functional control Spiegelmer on alternate days, starting from day 21 or 42 of age. Glomerular and interstitial macrophage counts were found to be reduced with Ccl2 blockade by 50% and 30%, respectively. However, this was not associated with an improvement of glomerular pathology, interstitial pathology, or of overall survival of <jats:italic>Col4a3<\/jats:italic>\u2010deficient mice. We conclude that Ccl2 mediates the recruitment of glomerular and interstitial macrophages but this mechanism does not contribute to the progression of Alport nephropathy in <jats:italic>Col4a3<\/jats:italic>\u2010deficient mice. Copyright \u00a9 2008 Pathological Society of Great Britain and Ireland. 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