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PATHWAYS OF SIGNAL TRANSDUCTION OF INTRACELLULAR Ca2 + INCREASE MEDIATED BY THREE SUBTYPES OF α1-ADRENOCEPTOR IN HEK293 CELLS
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- Author:
- No author available
- Journal Title:
- ACTA PHYSIOLOGICA SINICA
- Issue:
- 3
- DOI:
- 10.3321/j.issn:0371-0874.1998.03.018
- Key Word:
- α1-肾上腺素受体;受体亚型;G蛋白;磷脂酶C;蛋白激酶C;环-磷酸腺苷;酪氨酸激酶;fura-2
Abstract： 本文探讨了α1a,α1b,α1d三种亚型肾上腺素受体(AR)激动时细胞内Ca2+浓度([Ca2+]i)升高的信号转导途径.在稳定表达三亚型α1-AR的HEK293细胞系中,用fura-2方法描记细胞内Ca2+信号强弱的变化.结果显示,百日咳毒素(PTX)对去甲肾上腺素激动三亚型α1-AR而引起的[Ca2+]i升高无影响,U-73122和PMA明显抑制[Ca2+]i升高;Calphostin C和PMA过夜预处理可翻转PMA的抑制作用;Forskolin和Rp-cAMPs对α1-AR介导的[Ca2+]i升高无影响,但Quercetin和Tyrphostin可抑制[Ca2+]i升高峰值,对平台期幅值则无影响.因此,在HEK293细胞,三亚型α1-AR可通过PTX非敏感G蛋白激活PLC而介导磷酸肌醇-Ca2+信号系统,PKC磷酸化系统既抑制α1-AR介导的细胞内贮存Ca2+释放,又抑制细胞外Ca2+内流;cAMP系统不参与α1-AR介导Ca2+信号的调节,酪氨酸激酶可能参与这一过程.
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