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. Author manuscript; available in PMC: 2012 Jan 11.
Published in final edited form as: Toxicology. 2010 Oct 8;279(1-3):54–64. doi: 10.1016/j.tox.2010.09.007

Figure 6. Modifications in gene expression explain calcium handling dynamics in DEHP-treated cardiomyocytes.

Figure 6

(A) Control and DEHP-treated (50 μg/mL) cardiomyocytes were loaded with Fluo-4 to analyze calcium transient morphology. DEHP-treated samples showed a significant increase in calcium transient upstroke duration compared to control (left). In addition, a large number of traces show evidence of double transients, indicating increased arrhythmogenicity (center). Individual calcium transients recorded from control and DEHP-treated cardiomyocytes are shown on the right. (B) Numerous calcium handling genes were shown to be differentially expressed in DEHP-treated samples (50 μg/mL) versus control. Calponin (CNN1), troponin C (TNNC1), calsequestrin 2 (CASQ2) expression were decreased following DEHP treatment. Ryanodine receptor 2 (RYR2), cardiac calcium transporting ATPase (ATP2A2), triadin (TRDN), voltage-dependent l-type calcium channel (CACNA1C), phospholamban (PLN), sodium/potassium transporting ATPase β2 (ATP1B2) and cardiac myosin heavy chain (MYH6) expression were increased following DEHP treatment. (C) Cartoon illustrating key players involved in calcium handling within cardiomyocytes, which are modified following DEHP exposure.