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Xiaodan Ren, Cory Hogaboam, Audra Carpenter, Lisa Colletti
Published in Volume 112, Issue 9
J Clin Invest. 2003; 112(9):1407–1418 doi:10.1172/JCI17391
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Figure 5

BrdU staining following partial hepatectomy in (a) mice treated with anti-SCF or control antibody; (b) Sl/Sld or WT mice; and (c) Sl/Sld or WT mice treated with SCF or vehicle. Mice underwent 70% hepatectomy, and BrdU staining was used as an estimate of hepatocyte proliferation. The effects of anti-SCF or control antibody after partial hepatectomy are shown in a. Anti-SCF antibody treatment resulted in a significant decrease in hepatocyte proliferation at 48 and 60 hours after hepatectomy (*P < 0.05 vs. hepatectomy alone and hepatectomy plus control antibody). Interestingly, there is a significant rise in BrdU staining in anti–SCF-treated animals at 72 hours after hepatectomy, suggesting that blockade of SCF effects results in a delay in proliferation, although proliferation is not completely prevented (*P < 0.05 vs. hepatectomy alone and hepatectomy plus control antibody). The effects of hepatectomy in Sl/Sld or WT mice are illustrated in b. WT animals have significantly increased levels of hepatocyte proliferation compared with Sl/Sld mice, particularly at 48 and 60 hours after hepatectomy. Sl/Sld mice did demonstrate increasing proliferation at 72 hours postoperatively, suggesting that some rebound in proliferation was occurring. (*P < 0.05 vs. WT). The effects of exogenous SCF administration on Sl/Sld or WT mice after 70% hepatectomy are illustrated in c. SCF administration to WT animals had minimal effects; in contrast, SCF administration to Sl/Sld mice restored hepatocyte proliferation to near-normal. *P < 0.05 vs. WT mice treated with vehicle, WT mice treated with SCF, and Sl/Sld mice treated with SCF. LPF, low power field.