Endogenously released ATP mediates shear stress-induced Ca2+ influx into pulmonary artery endothelial cells Export

@article{yamamoto2003, abstract = {The mechanisms by which flow-imposed shear stress elevates intracellular Ca2+ in cultured endothelial cells (ECs) are not fully understood. Here we report finding that endogenously released ATP contributes to shear stress-induced Ca2+ responses. Application of flow of Hanks' balanced solution to human pulmonary artery ECs (HPAECs) elicited shear stress-dependent increases in Ca2+ concentrations. Chelation of extracellular Ca2+ with EGTA completely abolished the Ca2+ responses, whereas the phospholipase C inhibitor U-73122 or the Ca2+-ATPase inhibitor thapsigargin had no effect, which thereby indicates that the response was due to the influx of extracellular Ca2+. The Ca2+ influx was significantly suppressed by apyrase, which degrades ATP, or antisense oligonucleotide targeted to P2X4 purinoceptors. A luciferase luminometric assay showed that shear stress induced dose-dependent release of ATP. When the ATP release was inhibited by the ATP synthase inhibitors angiostatin or oligomycin, the Ca2+ influx was markedly suppressed but was restored by removal of these inhibitors or addition of extracellular ATP. These results suggest that shear stress stimulates HPAECs to release ATP, which activates Ca2+ influx via P2X4 receptors.}, author = {Yamamoto, Kimiko and Sokabe, Takaaki and Ohura, Norihiko and Nakatsuka, Hideki and Kamiya, Akira and Ando, Joji}, citeulike-article-id = {2334303}, citeulike-linkout-0 = {http://ajpheart.physiology.org/cgi/content/abstract/285/2/H793}, doi = {10.1152/ajpheart.01155.2002}, eprint = {http://ajpheart.physiology.org/cgi/reprint/285/2/H793.pdf}, journal = {Am J Physiol Heart Circ Physiol}, keywords = {atp, endothelial, experimental, invitro, wss}, number = {2}, pages = {H793--803}, pdf = {yamamoto2003.pdf}, posted-at = {2008-02-05 10:47:24}, priority = {0}, title = {{Endogenously released ATP mediates shear stress-induced Ca2+ influx into pulmonary artery endothelial cells}}, url = {10.1152/ajpheart.01155.2002}, volume = {285}, year = {2003} }

TY - JOUR ID - yamamoto2003 L3 - citeulike-article-id:2334303 N2 - The mechanisms by which flow-imposed shear stress elevates intracellular Ca2+ in cultured endothelial cells (ECs) are not fully understood. Here we report finding that endogenously released ATP contributes to shear stress-induced Ca2+ responses. Application of flow of Hanks' balanced solution to human pulmonary artery ECs (HPAECs) elicited shear stress-dependent increases in Ca2+ concentrations. Chelation of extracellular Ca2+ with EGTA completely abolished the Ca2+ responses, whereas the phospholipase C inhibitor U-73122 or the Ca2+-ATPase inhibitor thapsigargin had no effect, which thereby indicates that the response was due to the influx of extracellular Ca2+. The Ca2+ influx was significantly suppressed by apyrase, which degrades ATP, or antisense oligonucleotide targeted to P2X4 purinoceptors. A luciferase luminometric assay showed that shear stress induced dose-dependent release of ATP. When the ATP release was inhibited by the ATP synthase inhibitors angiostatin or oligomycin, the Ca2+ influx was markedly suppressed but was restored by removal of these inhibitors or addition of extracellular ATP. These results suggest that shear stress stimulates HPAECs to release ATP, which activates Ca2+ influx via P2X4 receptors. IS - 2 JF - Am J Physiol Heart Circ Physiol EP - 803 TI - {Endogenously released ATP mediates shear stress-induced Ca2+ influx into pulmonary artery endothelial cells} VL - 285 SP - H793 KW - atp KW - endothelial KW - experimental KW - invitro KW - wss AU - Yamamoto, Kimiko AU - Sokabe, Takaaki AU - Ohura, Norihiko AU - Nakatsuka, Hideki AU - Kamiya, Akira AU - Ando, Joji PY - 2003/// UR - http://ajpheart.physiology.org/cgi/content/abstract/285/2/H793 ER -