Fig 1: Cell tracking and distribution in mice treated with MSC or KIM-MSC. (A): KIM1 expression was upregulated in the STK 24 hours after induction of RAS, peaked at 48 hours, remained upregulated 2 weeks after, and was unaffected by the injection of KIM-MSC. KIM1 expression was minimal in the sham and CLK, scale bar = 100 µm. (B): Representative images of CM-DiI labeled (red) MSC in KIM1 (green)-stained STK and CLK 48 hours after delivery into the aorta (yellow arrow shows MSC colocalizing with endogenous KIM1-positive tubules, scale bar = 50 µm). (C): The STK consistently shows greater homing of MSC compared to the CLK, as well as about twice as many MSC colocalizing with KIM1 in RAS mice injected with KIM-MSC compared to native MSC. (D): FACS analysis showing the distribution of MSC 48 hours after injection, as a fraction of cellular content in each organ. KIM-MSC-treated mice showed the greatest MSC fraction in the STK compared to the CLK, lung, and liver, whereas mice treated with native MSC did not show a difference. #, p < .05 versus Sham, $, p < .05 versus 24 hours, *, p < .05 versus RAS+MSC, &, p < .05 versus RAS+KIM-MSC CLK, Lung, Liver. Abbreviations: CLK, contralateral kidney; FACS, fluorescence-activated cell sorting; KIM1, kidney injury molecule-1; MSC, mesenchymal stem cells; RAS, renal artery stenosis; STK, stenotic kidney.