Fig. 5: Bone marrow-derived cells with Ripk3 or Mlkl deficiency reduced renal fibrosis and inflammasome activation in progression of IRI to CKD.

Chimeric mice were created, in which the BM was replaced with donor BM cells from WT or from Ripk3^−/− or Mlkl^−/− mice. Irradiated Ripk3^+/+ and Ripk3^−/− mice were reconstituted with either Ripk3^+/+ or Ripk3^−/− BM cells, and similar experiments were performed in Mlkl background mice. a Representative kidney sections (Bar = 100 μM), and (b–d) quantification of renal injury in Ripk3 BM chimeric mice at 2,14 days and 2 months after IRI. n = 6. *P < 0.05,**P < 0.01 vs. RW to RW chimeric mice; ^##P < 0.01, vs. RK to RW chimeric mice; ^#P < 0.05, vs. RW to RK chimeric mice. f Representative kidney sections (Bar = 100 μM) and (g–i) quantification of renal injury in Mlkl BM chimeric mice at 2,14 days and 2 months after IRI. n = 6. *P < 0.05, **P < 0.01 vs. MW to MW chimeric mice; ^##P < 0.01, vs. MK to MW chimeric mice; ^#P < 0.05, vs. MW to MK chimeric mice. e, j Quantitative RT-PCR analysis for MCP-1 of the total kidney lysates from mice on 2 and 14 days after IRI. **P < 0.01, vs. RW to RW or MW to MW chimeric mice on day 2 IRI; ^∆P < 0.05, ^∆∆P < 0.01, vs. RW to RW or MW to MW IRI chimeric mice on day 14 IRI. n = 6. k, l Representative Western blot image of active caspase-1 and mature (processed) IL-1β were shown. GADPH was used as the loading control. n = 4. RW Ripk3^+/+, RK Ripk3^−/−, MW Mlkl^+/+, MK Mlkl^−/−