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首页> 外文期刊>Cellular Signalling >Involvement of aquaporin in thromboxane A(2) receptor-mediated, G(12/13)/RhoA/NHE-sensitive cell swelling in 1321N1 human astrocytoma cells
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Involvement of aquaporin in thromboxane A(2) receptor-mediated, G(12/13)/RhoA/NHE-sensitive cell swelling in 1321N1 human astrocytoma cells

机译：水通道蛋白参与1321N1人类星形细胞瘤细胞中血栓烷A（2）受体介导的G（12/13）/ RhoA / NHE敏感细胞肿胀

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The physiological role of the thromboxane A(2) (TXA(2)) receptor expressed on glial cells remains unclear. We previously reported that 1321N1 human astrocytoma cells pretreated with dibutyryl cyclic AMP (dbcAMP) became swollen in response to U46619, a TXA(2) analogue. In the present study, we examined the detailed mechanisms of TXA(2) receptor-mediated cell swelling in 1321N1 cells. The cell swelling caused by U46619 was suppressed by expression of p115-RGS, an inhibitory peptide of G alpha(12/13) pathway and C3 toxin, an inhibitory protein for RhoA. The swelling was also inhibited by treatment with Y27632, a Rho kinase inhibitor and 5-(ethyl-N-isopropyl)amiloride (EIPA), a Na+/H+-exchanger inhibitor. Furthermore, cell swelling was suppressed by the pretreatment with aquaporin inhibitors mercury chloride or phloretin in a concentration-dependent manner, suggesting that aquaporins are involved in U46619-induced 1321N1 cell swelling. In fact, U46619 caused [H-3]H2O influx into the cells, which was inhibited by p115-RGS, C3 toxin, EIPA, mercury chloride and phloretin. This is the first report that the TXA(2) receptor mediates water influx through aquaporins in astrocytoma cells via TXA(2) receptor-mediated activation of G alpha(12/13), Rho A, Rho kinase and Na+/H+-exchanger.
机译：在胶质细胞上表达的血栓烷A（2）（TXA（2））受体的生理作用仍然不清楚。我们以前曾报道过，用丁酸环状AMP（dbcAMP）预处理的1321N1人星形细胞瘤细胞在响应U46619（一种TXA（2）类似物）时变得肿胀。在本研究中，我们检查了1321N1细胞中TXA（2）受体介导的细胞肿胀的详细机制。 U46619引起的细胞肿胀被p115-RGS（G alpha（12/13）途径的抑制肽）和C3毒素（RhoA的抑制蛋白）的表达抑制。通过用Rho激酶抑制剂Y27632和Na + / H +交换抑制剂5-（乙基-N-异丙基）阿米洛利（EIPA）处理也可以抑制肿胀。此外，通过水通道蛋白抑制剂氯化汞或促绿素原的预处理以浓度依赖的方式抑制了细胞肿胀，这表明水通道蛋白参与了U46619诱导的1321N1细胞肿胀。实际上，U46619导致[H-3] H2O流入细胞，并被p115-RGS，C3毒素，EIPA，氯化汞和促视紫红质抑制。这是第一个报告TXA（2）受体通过TXA（2）受体介导的G alpha（12/13），Rho A，Rho激酶和Na + / H +交换子激活通过星形胶质细胞瘤中的水通道蛋白介导水流入。

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