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. 2016 Jan 11;11(1):e0146554. doi: 10.1371/journal.pone.0146554

Fig 3. M. fortuitum alters intracellular Ca+2 homeostasis leading to activation of CaM and PKC-α.

Fig 3

(A) HKM were pre-treated with or without BAPTA/AM followed by M. fortuitum infection and cytosolic Ca+2 elevation was measured using Fluo-4 at 1 h of infection. (B) HKM transfected with indicated siRNA or pre-treated separately with indicated inhibitors and at 4 h p.i. CaM-protein expression detected by EIA. (C) Fold changes in CaM-mRNA expression was determined in HKM transfected with specific siRNA or non-targeted siRNA followed by M. fortuitum infection 4 h p.i by qPCR. (D) HKM were pre-treated separately with or without indicated inhibitors and PKC activity determined at 2 h p.i. Vertical bars represent mean ± SE (n = 3).*P<0.05, compared to HKM; γP<0.05, compared to HKM+Sc; #P<0.05, compared to HKM+MF; •P<0.05, compared to HKM+MF+Sc. HKM, control head kidney macrophage; HKM+Sc, HKM transfected with scrambled siRNA; HKM+MF, HKM infected with M. fortuitum; HKM+MF+Sc, HKM transfected with scrambled siRNA infected with M. fortuitum; HKM+MF+siRNA-CaM, HKM transfected with siRNA-CaM infected with M. fortuitum; HKM+MF+BAPTA/AM, HKM+MF+CMZ, HKM+MF+CC, HKM+MF+Gö6976, HKM were pre treated with BAPTA/AM, CMZ, CC, Gö6979 respectively followed by infection with M. fortuitum.