Aragay A M, Mellado M, Frade J M, Martin A M, Jimenez-Sainz M C, Martinez-A C, Mayor F
Departamento de Biologia Molecular, Centro de Biologia Molecular "Severo Ochoa,", Universidad Autonoma de Madrid, Campus Cantoblanco, E-28049 Madrid, Spain.
Proc Natl Acad Sci U S A. 1998 Mar 17;95(6):2985-90. doi: 10.1073/pnas.95.6.2985.
Monocyte chemoattractant protein 1 (MCP-1) is a member of the chemokine cytokine family, whose physiological function is mediated by binding to the CCR2 and CCR4 receptors, which are members of the G protein-coupled receptor family. MCP-1 plays a critical role in both activation and migration of leukocytes. Rapid chemokine receptor desensitization is very likely essential for accurate chemotaxis. In this report, we show that MCP-1 binding to the CCR2 receptor in Mono Mac 1 cells promotes the rapid desensitization of MCP-1-induced calcium flux responses. This desensitization correlates with the Ser/Thr phosphorylation of the receptor and with the transient translocation of the G protein-coupled receptor kinase 2 (GRK2, also called beta-adrenergic kinase 1 or betaARK1) to the membrane. We also demonstrate that GRK2 and the uncoupling protein beta-arrestin associate with the receptor, forming a macromolecular complex shortly after MCP-1 binding. Calcium flux responses to MCP-1 in HEK293 cells expressing the CCR2B receptor were also markedly reduced upon cotransfection with GRK2 or the homologous kinase GRK3. Nevertheless, expression of the GRK2 dominant-negative mutant betaARK-K220R did not affect the initial calcium response, but favored receptor response to a subsequent challenge by agonists. The modulation of the CCR2B receptor by GRK2 suggests an important role for this kinase in the regulation of monocyte and lymphocyte response to chemokines.
单核细胞趋化蛋白1(MCP-1)是趋化因子细胞因子家族的成员,其生理功能通过与G蛋白偶联受体家族成员CCR2和CCR4受体结合来介导。MCP-1在白细胞的激活和迁移中都起着关键作用。趋化因子受体的快速脱敏很可能对精确的趋化性至关重要。在本报告中,我们表明MCP-1与单核巨噬细胞1细胞中的CCR2受体结合可促进MCP-1诱导的钙流反应的快速脱敏。这种脱敏与受体的丝氨酸/苏氨酸磷酸化以及G蛋白偶联受体激酶2(GRK2,也称为β-肾上腺素能激酶1或βARK1)向膜的短暂转位相关。我们还证明,GRK2和解偶联蛋白β-抑制蛋白与受体结合,在MCP-1结合后不久形成大分子复合物。在与GRK2或同源激酶GRK3共转染后,表达CCR2B受体的HEK293细胞中对MCP-1的钙流反应也明显降低。然而,GRK2显性负突变体βARK-K220R的表达并不影响初始钙反应,但有利于受体对激动剂随后刺激的反应。GRK2对CCR2B受体的调节表明该激酶在调节单核细胞和淋巴细胞对趋化因子的反应中起重要作用。