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. Author manuscript; available in PMC: 2015 Dec 1.
Published in final edited form as: J Mol Med (Berl). 2014 Sep 25;92(12):1245–1256. doi: 10.1007/s00109-014-1209-3

Figure 4.

Figure 4

Diabetes-induced pro-inflammatory and pro-fibrotic gene expression in the kidney, and urinary excretion of cytokines, is diminished in sema3A KO mice. A. Inflammatory cytokine and chemokine expression in kidney was significantly increased in WT diabetic mice and blunted by sema3A gene deletion. *, p<0.001 vs. other groups. B. Expression of profibrotic genes collagen I, CTGF and TGFβ1 is significantly induced in kidneys of WT diabetic mice as compared to control mice; sema3A gene deletion reduced collagen I and TGFβ1 but not CTGF expression. *, p<0.05 vs. other groups. IL- 6 excretion (C) and MCP-1 (D) excretion in urine was significantly increased by diabetes in WT mice, which was reduced in sema3A KO mice. *, p<0.001 vs. control. #, p<0.05 vs. WT diabetic animals. Expression of sema3A (E) and sema3A receptors (F) in kidneys of control and diabetic mice. Both sema3A and several of its receptors were induced by diabetes in WT mice, which was blunted in sema3A KO mice. *, p<0.001 vs. other groups. #, p<0.05 vs. control. n=6–8.