@article{oai:soar-ir.repo.nii.ac.jp:00004169,
 author = {TSUJINO, Natsuko and NAKADA, Tsutomu and TSUBOUCHI, Kiyotaka and KOBAYASHI, Masaaki and KAWAI, Yoshiko and YANO, Shiharu and ATSUNAGA, Tamihide and HIROSE, Masamichi and OHMORI, Shigeru and OHHASHI,  Toshio and YAMADA,  Mitsuhiko},
 issue = {1},
 journal = {信州医学雑誌},
 month = {Feb},
 note = {We analyzed Ca-permeating nonselective cation channels (NSCs)mediating thrombin-induced contraction of human umbilical vein endothelial cells (HUVECs). A Ca chelater, BAPTA-AM (10μM), significantly inhibited the thrombin-induced contraction of HUVECs.Thrombin induced inward currents at -60 mV in the presence of intracellular MgATP. Removal of extracellular Caﾌﾞｸﾞsignificantly decreased the currents. A selective phospholipase C inhibitor, U73122 (1μM) but not its inactive analogue, U73343 (1μM) almost completely inhibited the currents. Neither a selective inhibitor of Caﾌﾞｸﾞ-ATPase of endoplasmic reticulum, thapsigargin (1μM)nor a diacylglycerol analogue, 1-oleoyl-2-acetyl-glycerol (30μM)activated the currents. However, a selective protein kinase C inhibitor, bisindolylmaleimide I (500 nM) significantly inhibited the currents.The thrombin-induced currents were significantly inhibited by SKF96365 (50μM)but not by La(1mM), ruthenium red (10μM) or flufenamic acid (100μM). As assessed with RT-PCR, HUVECs expressed transient receptor potential(TRP)M4,7,TRPV1,2,4,TRPC1,4 and 6 subunits of NSCs.These results indicate that thrombin activates Ca-permeating NSCs containing TRPC4 through protein kinase C in HUVECs. Thus,drugs specifically inhibiting TRPC4-containing channels might be effective to control fatal diseases such as sepsis where thrombin mediates the vicious cycle between inflammation and coagulation., Article, 信州医学雑誌 59(1): 13-26(2011)},
 pages = {13--26},
 title = {Thrombin Activates Ca2+-permeating Nonselective Cation Channels through Protein Kinase C in Human Umbilical Vein Endothelial Cells},
 volume = {59},
 year = {2011}
}