Deletion of p38α ameliorates tubular but not glomerular damage during anti-GBM nephritis.

<p>(A) Semi-quantitative scoring of tubular damage. p38α deletion significantly diminishes tubular damage (mean score 0.6±0.1, p<0.05 vs. control; n = 7) as compared to wild type mice (mean score 0.9±0.01; n = 7). Tubules of wild type mice (B) are dilated, whereas tubules of <i>MxCre-p38α^Δ/Δ</i> (C) mice are still tightly packed. (D) KIM-1 mRNA level is dramatically increased in wild type mice (wild type 84.23±32.57; n = 4 vs. <i>p38α^Δ/Δ</i> 2.675±1.248; n = 4) indicating high tubular damage. (E) Vimentin shows clear upregulation of its mRNA in wild type mice (2.900±0.1732; n = 4) whereas it is reduced nearly to the baseline level in <i>MxCre-p38α^Δ/Δ</i> mice (1.375±0.3497; n = 4). Dashed line indicates RNA base level of control mice. (F–H) Analysis of crescent formation during anti GBM nephritis. Similar amounts of glomeruli revealed crescent formation in wild type (n = 6) and <i>MxCre-p38α^Δ/Δ</i> mice (n = 6) (wild type: mean 3.3±1.2% vs. <i>MxCre-p38α^Δ/Δ</i>: 4.2±1.5, p = ns). (I–K) Fibrotic tissue remodelling occurred in both wild type (n = 7) and <i>MxCre-p38α^Δ/Δ</i> mice (n = 7) (wild-type: mean 1.409±0.1132 vs <i>MxCre-p38α^Δ/Δ</i>: 1.615±0.1617, p = ns). Sirius red staining was performed 14 days after induction of anti-GBM nephritis. (L–M) p38α deletion affects the immune response to sheep IgG by decreased murine IgG depositions in the glomeruli.