Kim Min Suk, Lee Jinhwa, Ha Joohun, Kim Sung Soo, Kong Yoon, Cho Yong Ho, Baik Hyung Hwan, Kang Insug
Department of Biochemistry, School of Medicine, Kyung Hee University, 1 Hoegi-dong, Dongdaemun-ku, Seoul 130-701, Republic of Korea.
Arch Biochem Biophys. 2002 May 15;401(2):205-14. doi: 10.1016/S0003-9861(02)00056-5.
Extracellular ATP acts as a signal that regulates a variety of cellular processes via binding to P2 purinergic receptors (P2 receptors). We herein investigated the effects and signaling pathways of ATP on glucose uptake in C(2)C(12) skeletal muscle cells. ATP as well as P2 receptor agonists (ATP-gamma S) stimulated the rate of glucose uptake, while P2 receptor antagonists (suramin) inhibited the stimulatory effect of ATP, indicating that P2 receptors are involved. This ATP-stimulated glucose transport was blocked by specific inhibitors of Gi protein (pertusiss toxin), phospholipase C (U73122), protein kinase C (GF109203X), and phosphatidylinositol (PI) 3-kinase (LY294002). ATP stimulated PI 3-kinase activity and P2 receptor antagonists blocked this activation. In C(2)C(12) myotubes expressing glucose transporter GLUT4, ATP increased basal and insulin-stimulated glucose transport. Finally, ATP facilitated translocation of GLUT1 and GLUT4 into plasma membrane. These results together suggest that cells respond to extracellular ATP to increase glucose transport through P2 receptors.
细胞外ATP作为一种信号，通过与P2嘌呤能受体（P2受体）结合来调节多种细胞过程。我们在此研究了ATP对C2C12骨骼肌细胞葡萄糖摄取的影响及其信号通路。ATP以及P2受体激动剂（ATP-γS）刺激了葡萄糖摄取速率，而P2受体拮抗剂（苏拉明）抑制了ATP的刺激作用，表明P2受体参与其中。这种ATP刺激的葡萄糖转运被Gi蛋白特异性抑制剂（百日咳毒素）、磷脂酶C（U73122）、蛋白激酶C（GF109203X）和磷脂酰肌醇（PI）3激酶（LY294002）阻断。ATP刺激PI 3激酶活性，P2受体拮抗剂阻断这种激活。在表达葡萄糖转运蛋白GLUT4的C2C12肌管中，ATP增加基础和胰岛素刺激的葡萄糖转运。最后，ATP促进GLUT1和GLUT4向质膜的转位。这些结果共同表明，细胞通过P2受体对细胞外ATP作出反应以增加葡萄糖转运。
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