@article{oai:hirosaki.repo.nii.ac.jp:00003840,
 author = {Murakami, Kazuo and Osanai, Tomohiro and Tanaka, Makoto and Kinjo, Takahiko and Tanno, Tomohiro and Narita, Ikuyo and Kawai, Misato and Tomita, Hirofumi and Okumura, Ken},
 issue = {1},
 journal = {弘前医学},
 month = {Apr},
 note = {Background: We reported that enhanced phospholipase C （PLC）-δ1, which was detected in patients with coronary spasm, caused coronary spasm in mice. We investigated the role of protein kinase C（ PKC） in acetylcholine （ACh）-induced Ca2+ influx under enhanced PLC-δ1 using human embryonic kidney（ HEK）-293 cells. Methods and Results: Intracellular free Ca2+ concentration （[Ca2+]i） was measured by fura-2, and Ca2+ influx was evaluated by the increase in [Ca2+]i after addition of extracellular Ca2+. ACh-induced Ca2+ influx（ nM） in HEK-293 cells was 21±2 in control HEK-293 cells, 52±6 in the cells with PLC-δ1 overexpression, and 75±9 in those with PLC-δ1 overexpression and PKC down-regulation （all p<0.05 among 3 groups）. Ca2+ influx under treatment with nifedipine at 10-5M was 2.9±0.1 times higher in the cells with PLC-δ1 overexpression and 5.6±0.2 times higher in those with PLC-δ1 overexpression and PKC down-regulation compared with the control cells（ all p<0.05 among 3 groups）. Conclusions: ACh-induced Ca2+ influx was enhanced by PLC-δ1 overexpression, but was attenuated by PKC activation. PKC plays an important role in Ca2+ influx under enhanced PLC-δ1 in a negative feedback fashion., 弘前医学. 66, 2015, p.22-27},
 pages = {22--27},
 title = {Role of Protein Kinase C in Acetylcholine-Induced Ca2+ Influx under Enhanced Phospholipase C-δ1},
 volume = {66},
 year = {2015}
}