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. 2019 Jun 4;13(1):192–206. doi: 10.1080/19336950.2019.1623591

Figure 1.

Figure 1.

TRPA1 stimulation elicits Akt and eNOS phosphorylation concomitantly with nitric oxide (NO) production in CMs. (a) Representative immunoblots and (b) fluorescent images depicting the time-dependent effects of AITC (100 µM) on Akt serine 473 and eNOS serine 1177 phosphorylation (AktpS473 and eNOSpS1177, respectively) and NO production in wild-type (WT) and TRPA1 knockout (TRPA1-/-) cardiomyocytes (CMs) measured at 0, 2, 5, 10 min. Total Akt and eNOS were probed as loading controls for immunoblots. (A’) Summarized data for Figure 1(a) and (B’) Figure 1(b). Immunoblot data are expressed as a percent of the untreated mean control values (phosphorylated protein/total amount of respective protein) ± SEM, whereas NO data are expressed as percent relative fluorescent units (RFU) of the untreated WT mean control value ± SEM. N = CMs obtained from four different hearts. *p < 0.05, **p < 0.01, ***p < 0.001 compared to mean control value. (c) Summarized nitrite assay data depicting the effects of AITC (0–300 µM) and vehicle (Veh; EtOH) on nitrite production in CMs obtained from WT and TRPA1-/- hearts. Absorbance was recorded at 540 nm. Data are expressed as the amount of nitrite produced per mg of sample protein. N = CMs obtained from four different hearts and data collected from 10 assays. *p < 0.05, **p < 0.01, ***p < 0.001 compared to vehicle-treated control value within the respective CM cohorts.