Trends in Pharmacological Sciences
Receptor sites for Ca2+ channel antagonists
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Design, synthesis, and anticancer activity of iridium(III) complex-peptide hybrids that contain hydrophobic acyl groups at the N-terminus of the peptide units
2019, Journal of Inorganic BiochemistryCitation Excerpt :It is described that programed cell death can be classified into apoptosis, necroptosis, paraptosis, autophagic cell death, and so on [26–51]. In our previous study, we reported that cell death induced by 3a (with a peptide at the 5′-position) was not inhibited by a broad caspase inhibitor, Z-VAD-fmk [18], while inhibition was observed in the presence some inhibitors related to Ca2+ homeostasis including 3-chlorophenylhydrazone (CCCP, an uncoupling reagent and an inhibitor of mitochondrial Ca2+ uptake) [44,45], verapamil (an L-type voltage-operated Ca2+ channel blocker) [46–48], quinidine (a Na+ and K+ channel blocker) [49,50] and xestospongin C (a selective inhibitor of the IP3 receptor on the ER which releases Ca2+ into the cytosol) [51,52]. Based on these data, it was concluded that 3a negligibly induces apoptosis but involves cell death that is mediated by Ca2+-dependent signaling pathways.
A cell-based assay for the detection of pathogenic anti-voltage-gated calcium channel autoantibodies in immunoglobulin G from patients with type 1 diabetes
2018, Journal of Immunological MethodsCitation Excerpt :Co-incubation of cells with both Bay K8644 and nicardipine reduced the number of DCF-DA positive cells compared to Bay K8644 alone, with a significant reduction in DCF-DA positive cells achieved at 10 nM nicardipine (Fig. 1 B). Previous studies have demonstrated that the serum, or the IgG fraction, from patients with T1D contains a functional Ab that acts as an agonist at the DHP binding site of L-Type VGCCs, and disrupts channel-mediated physiological responses in live tissue or cell-based assays (Catterall and Striessnig, 1992; Jackson et al., 2004; Jackson and Gordon, 2010). Recent reports indicate that these anti-VGCC Abs are capable of mediating over-activity of VGCCs in cultured pancreatic β cell lines, resulting in altered ion exchange and induction of apoptosis (Chang et al., 2004; Bason et al., 2013; Yang et al., 2015).
Use of calcium channel blockers for glaucoma
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