{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,22]],"date-time":"2025-10-22T00:32:40Z","timestamp":1761093160314,"version":"build-2065373602"},"reference-count":34,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2008,1,10]],"date-time":"2008-01-10T00:00:00Z","timestamp":1199923200000},"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":[[2008,4]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Fetal mesenchymal stem cell (fetal MSC) therapy has potential to treat genetic diseases with early onset, including those affecting the kidney and urinary tract. A collagen type I\u03b12\u2010deficient mouse has a deletion in the \u03b12 chain of the procollagen type I gene, resulting in the synthesis of abnormal \u03b11(I)<jats:sub>3<\/jats:sub> homotrimers, which replace normal \u03b11(I)<jats:sub>2<\/jats:sub>\u03b12(I)<jats:sub>1<\/jats:sub> heterotrimers and a glomerulopathy. We first confirmed that <jats:italic>col1<\/jats:italic>\u03b1<jats:italic>2<\/jats:italic>\u2010deficient homozygous mice show abnormal collagen deposition in the glomeruli, which increases in frequency and severity with postnatal age. Intrauterine transplantation of human MSCs from first trimester fetal blood led postnatally to a reduction of abnormal homotrimeric collagen type I deposition in the glomeruli of 4\u201312 week\u2010old <jats:italic>col1<\/jats:italic>\u03b1<jats:italic>2<\/jats:italic>\u2010deficient mice. Using bioluminescence imaging, <jats:italic>in situ<\/jats:italic> hybridization and immunohistochemistry in transplanted <jats:italic>col1<\/jats:italic>\u03b1<jats:italic>2<\/jats:italic>\u2010deficient mice, we showed that the damaged kidneys preferentially recruited donor cells in glomeruli, around mesangial cells. Real\u2010time RT\u2013PCR demonstrated that this effect was seen at an engraftment level of 1% of total cells in the kidney, albeit higher in glomeruli. We conclude that intrauterine transplantation of human fetal MSCs improves renal glomerulopathy in a collagen type I\u2010deficient mouse model. These data support the feasibility of prenatal treatment for hereditary renal diseases. Copyright \u00a9 2008 Pathological Society of Great Britain and Ireland. 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