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. Author manuscript; available in PMC: 2017 Jun 1.
Published in final edited form as: Atherosclerosis. 2016 Mar 26;249:1–9. doi: 10.1016/j.atherosclerosis.2016.03.032

Fig. 4. Intracellular Ca2+ handling is biphasically altered with CAD severity.

Fig. 4

(A) Experimental protocol for panels B–E. (B) The caffeine-sensitive steady-state SR store is increased in mild CAD compared to both healthy lean and severe CAD. (C) The undershoot of cytosolic Ca2+ during recovery following removal of caffeine (SERCA activity) is increased in mild CAD compared to both healthy lean and severe CAD. (D) When compared with CSM isolated from the adjacent arterial media (wall), intimal (plaque) CSM display decreased caffeine-releasable steady-state SR Ca2+ store. (E) When compared with CSM isolated from the adjacent arterial media (wall), intimal (plaque) CSM display decreased SERCA activity. (Healthy = 6 pigs, cells = 67; Mild CAD = 9 pigs, cells = 156; Plaque = 5 pigs, cells = 29; Wall = 5 pigs, cells = 27). (F) Experimental protocol for panels G–H. G. Rate of Ba2+ influx following depolarization is increased in CSM from mild CAD vs. Healthy and Severe CAD. (H) When compared to CSM from the media (wall) adjacent to the plaque, intimal (plaque) cells do not demonstrate a difference in Ba2+ influx. (Healthy = 6 pigs, cells = 72; Mild CAD = 9 pigs, cells = 151; Plaque = 5 pigs, cells = 25; Wall = 5 pigs, cells = 42). (I) Schematic depicting proposed changes in Ca2+ handling associated with CSM phenotypic modulation during CAD progression. Blue circles = Ca2+.