S. Kudo, M. Hosobuchi, Shogo Kuretoko, Tateki Sumii, Tomoya Shimada, Marie Terada, K. Tanishita
{"title":"Intercellular Ca 2+ response triggered by IP 3 among endothelial cells in shear stress flow","authors":"S. Kudo, M. Hosobuchi, Shogo Kuretoko, Tateki Sumii, Tomoya Shimada, Marie Terada, K. Tanishita","doi":"10.1299/KIKAIB.77.2431","DOIUrl":null,"url":null,"abstract":"A phenomenon has been observed in which intracellular Ca2+ concentration in endothelial cells increases upon application of shear stress (Ca2+ response). It is therefore assumed that Ca2+ is the second messenger in the transfer of shear stress stimulation into cells. The Ca2+ response is also known to spread to surrounding cells (Ca2+ wave). We investigated the effects on Ca2+ wave among cultured bovine aorta endothelial cells (BAECs) upon inhibiting the main intercellular signaling pathways, such as gap junction and paracrine pathways by inducing Ca2+ wave using D-myo-inositol 1,4,5-trisphosphate, P4(5)-(1-(2-nitrophenyl)ethyl) ester trisodium salt (Caged IP3) due to an intracellular IP3 elevation. In addition, we investigated the Ca2+ wave among BAECs under shear stress loading. Using Caged IP3, local release of ATP from BAEC induced Ca2+ wave. The Ca2+ wave was inhibited by the inhibitors of paracrine pathways. Furthermore, the Ca2+ response spread in the direction of the downstream under shear flow. These results suggest that paracrine pathway is dominant in both of flow and no flow conditions.","PeriodicalId":331123,"journal":{"name":"Transactions of the Japan Society of Mechanical Engineers. B","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2011-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Transactions of the Japan Society of Mechanical Engineers. B","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1299/KIKAIB.77.2431","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
A phenomenon has been observed in which intracellular Ca2+ concentration in endothelial cells increases upon application of shear stress (Ca2+ response). It is therefore assumed that Ca2+ is the second messenger in the transfer of shear stress stimulation into cells. The Ca2+ response is also known to spread to surrounding cells (Ca2+ wave). We investigated the effects on Ca2+ wave among cultured bovine aorta endothelial cells (BAECs) upon inhibiting the main intercellular signaling pathways, such as gap junction and paracrine pathways by inducing Ca2+ wave using D-myo-inositol 1,4,5-trisphosphate, P4(5)-(1-(2-nitrophenyl)ethyl) ester trisodium salt (Caged IP3) due to an intracellular IP3 elevation. In addition, we investigated the Ca2+ wave among BAECs under shear stress loading. Using Caged IP3, local release of ATP from BAEC induced Ca2+ wave. The Ca2+ wave was inhibited by the inhibitors of paracrine pathways. Furthermore, the Ca2+ response spread in the direction of the downstream under shear flow. These results suggest that paracrine pathway is dominant in both of flow and no flow conditions.