Fig. 2.
Knockdown of CK2α specifically augments M3R-mediated insulin secretion in MIN6 cells. Insulin release assays were carried out with MIN6 cells that had been treated with CK2α siRNA or scrambled control siRNA. (A–D) Cells were incubated with increasing concentrations of OXO-M (acting on endogenous M3Rs) (A), AVP (acting on endogenous V1B receptors) (B), glucose (C), or glibenclamide (D), an inhibitor of ATP-sensitive K+ channels. CK2α knockdown greatly enhanced M3R-mediated insulin release but had little or no effect on AVP-, glucose-, or glibenclamide-induced insulin secretion. Note that basal insulin secretion was slightly increased (P < 0.05) in cells treated with CK2α siRNA (insulin in ng/mL; control siRNA vs. CK2α siRNA: (A) 23.2 ± 1.5 vs. 28.1 ± 1.2; (B) 23.2 ± 1.6 vs. 28.2 ± 0.8; (C) 16.6 ± 0.6 vs. 22.0 ± 0.8; (D) 27.3 ± 0.6 vs. 31.0 ± 1.0. Data are expressed as the percentage increase in insulin release above basal levels and represent means ± SEM from three independent experiments. *P < 0.05, **P < 0.01, ***P < 0.001, compared with the corresponding control value.