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. 2021 Aug 17;9(8):1026. doi: 10.3390/biomedicines9081026

Figure 4.

Figure 4

KCNJ5 157-159delITE mutation increased CYP11B2 expression and aldosterone production through calcium-mediated pathway. The HAC15 cells were transiently transfected with wild-type or mutant KCNJ5. At 72 h after transfection, the samples and culture medium were collected and analyzed. (A) The CYP11B2 and KCNJ5 protein expression of cells harboring KCNJ5 mutant were significantly more than wild-type cells. The macrolides, clarithromycin or roxithromycin did not affect the CYP11B2 expression of cells harboring the KCNJ5 mutant. (B) The aldosterone production of cells harboring KCNJ5 mutant was significantly more than wild-type cells. The clarithromycin could partially inhibit aldosterone production of the KCNJ5 mutant cells. However, the roxithromycin could not inhibit aldosterone production of KCNJ5 mutant cells. Aldosterone production from HAC15 were adjusted by total protein. * indicated p < 0.05 vs. wild-type KCNJ5 group, # indicated p < 0.05 vs. 157-159delITE group. The macrolides were used as the inhibitors of mutant KCNJ5 channel. Nifedipine was used as inhibitor of downstream of KCNJ5-related pathway. Angiotensin II was a stimulator of aldosterone production.