Fig 2.
Luminal stenosis and negative remodeling are aggravated in canonical transient receptor potential 6 deficient (TRPC6-/-) mice after carotid wire injury. A, Wild-type (WT) and TRPC6-/- mice were subjected to carotid wire injury using either a 0.014-inch (n = 7 WT and n = 4 TRPC6-/- mice) or 0.018-inch (n = 0 WT and n = 2 TRPC6-/- mice) wire to produce cohorts with statistically similar percent CCA dilation. Filled circles designate mice injured with an 0.014-inch wire. Open circles designate mice injured with an 0.018-inch wire. B, Representative hematoxylin and eosin staining of WT and TRPC6-/- uninjured and injured CCA 28 days after carotid wire injury. C-F, WT (n = 7 mice) and TRPC6-/- (n = 6 mice) mice were analyzed at 28 days after injury. Filled and open circles correspond to mice injured with 0.014-inch and 0.018-inch wires, respectively. C, Luminal area in uninjured and injured WT and TRPC6-/- mice at 28 days after carotid wire injury. D, Percent change in luminal area in injured WT and TRPC6-/- CCA after carotid wire injury. E, The percent change in the area inside the external elastic lamina (EEL). F, The percent change in medial thickness.