Fig. 1.

Development of STZ-induced DKD in transient receptor potential canonical 6 (Trpc6) knockout and wild-type (WT) rats during the 11-wk protocol. A: scheme of WT TRPC6 and truncated TRPC6-m1 (SS^Trpc6−/−), which resulted from a 2-bp insertion leading to a frameshift mutation. B: protocol used for all four experimental groups (vehicle or STZ-treated WT and SS^Trpc6−/− rats). C: RT-PCR quantification of Trpc6 and Trpc5 mRNA expression in WT and SS^Trpc6−/− rats treated and not treated with STZ (values normalized to 18S); n = 4 rats for SS^WT, SS^Trpc6−/−, STZ-SS^WT, and STZ-SS^Trpc6−/−. D–F: development of diabetes in SS and SS^Trpc6−/− rats during the 11 wk after STZ injection observed by weight (D), blood glucose (E), and urinary output changes (F). n = 5, 18, 9, and 17 rats for SS^WT, SS^Trpc6−/−, STZ-SS^WT, and STZ-SS^Trpc6−/−, respectively. *P < 0.05 for SS^WT versus STZ-SS^WT, #P < 0.05 for SS^WT versus STZ-SS^Trpc6−/−, †P < 0.05 for SS^Trpc6−/− versus STZ-SS^Trpc6−/−, ‡P < 0.05 for SS^Trpc6−/− versus STZ-SS^WT. DKD, diabetic kidney disease; GFR, glomerular filtration rate; SS, salt-sensitive; STZ, streptozotocin.