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. 2017 Aug 8;7:7511. doi: 10.1038/s41598-017-07903-4

Figure 1.

Figure 1

TRPC6 deletion attenuates pressure overload-induced cardiac fibrosis but not fibrotic gene expression in mice. (a) Heart weight (HW) /body weight (BW) ratio in WT and TRPC6(−/−) mice 6 weeks after TAC. WT- TAC(−) (sham) (n = 6), TRPC6(−/−)-sham (n = 6), WT-TAC (n = 13), TRPC6(−/−)-TAC (n = 11). (b) Representative images of wheat germ agglutinin (WGA) staining for cross-sectional areas (CSA) measurement 6 weeks after TAC (left). Green; WGA, blue; DAPI. Quantitative results are shown in right panel. WT-sham (n = 6), TRPC6(−/−)-sham (n = 6), WT-TAC (n = 13), TRPC6(−/−)-TAC (n = 11). (c,d) TRPC6 contributes to TAC induced cardiac fibrosis. (c) Representative images of picrosirius red staining 6 weeks after TAC and results of interstitial fibrosis 6 weeks after TAC. WT-sham (n = 6), TRPC6(−/−)-sham (n = 6), WT-TAC (n = 13), TRPC6(−/−)-TAC (n = 11). (d) Relationship between fibrosis and hypertrophy 6 weeks after TAC. WT-sham (n = 6), TRPC6(−/−)-sham (n = 6), WT-TAC (n = 13), TRPC6(−/−)-TAC (n = 11). (e) Absence of TRPC6 does not affect pressure overload-induced LV dysfunction. LV end-diastolic pressure (LVEDP; left), LV end-systolic pressure (LVESP; middle) and LV dP/dtmax (right) in mice 6 weeks after TAC. WT-sham (n = 6), TRPC6(−/−)-sham (n = 6), WT-TAC (n = 13), TRPC6(−/−)-TAC (n = 11). (f) Expression levels of hypertrophy-related and fibrosis-related mRNAs in mouse hearts 1 week after TAC. WT-sham (n = 3), other groups (n = 4 each). Error bars, s.e.m. *P < 0.05, **P < 0.01. Results of WT mice were the same as those reported previously17, 18.