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. 2010 Oct 26;89(3):614–622. doi: 10.1093/cvr/cvq338

Figure 3.

Figure 3

ET-1-induced phosphorylation of MYPT-1 (Thr853), CPI-17 (Thr38), and MLC (Thr18/Ser19) is not observed when VSMCs are treated with the OGT inhibitor ST045849 or the ETA antagonist atrasentan. (A) Incubation of VSMCs with ET-1 (0.1 μM), ST045849 or atrasentan did not change expression of ROCK-α, ROCK-β, MYPT-1, MLC, or CPI-17. ET-1 increased expression of the phosphorylated forms of (B) CPI-17 (Thr38), (C) MLC (Thr18/Ser19), and (D) MYPT-1 (Thr853), an effect that was not observed when VSMCs were treated with the OGT inhibitor [ST045849]. In addition, treatment with the ETA antagonist (atrasentan) prevented ET-1-induced increased expression of the phosphorylated forms of (A) CPI-17, (B) MLC and (C) MYPT-1. Bar graphs show the relative expression of P-MYPT-1 (Thr853), P-CPI-17 (Thr38), or P-MLC (Thr18/Ser19) after normalization to corresponding total protein expression (n = 6). Results are presented as mean ± SEM in each experimental group. *P < 0.05 vs. control.