Figure 7.

Treatment of Alport mice with Ab2 reduces myofibroblasts and fibrosis in the interstitium of Alport kidneys. Cryosections either control mice (A and B), IgM-treated Alport mice (C and D), or Alport mice treated with Ab2 (E and F) or nonreactive isotype matched control antibody (IgM; C and D) were immunostained with antibodies against either smooth muscle actin (SMA, A, C, and E) or fibronectin (FN, B, D, and F). Both myofibroblast accumulation (SMA immunostaining) and fibrosis (as determined by fibronectin immunostaining) are markedly attenuated in renal cortex of Ab2-treated mice relative to the IgM-treated mice. Arrow in E denotes small focus of accumulating myofibroblasts in kidney cryosection from the treated animals. The fields shown are representative of 10 independent animals. Bar graphs at bottom represent semiquantitative assessment of the influence of Ab2 treatment in Alport mice from 4 to 7 seeks of age on glomerular sclerosis (left panel) and interstitial fibrosis (right panel). Bars represent statistically analyzed stat comprising three fields for five mice in each group (IgM versus Ab2).