MacLaughlin M, Martinez-Salgado C, Eleno N, Olivera A, Lopez-Novoa J M
Instituto Reina Sofía de Investigacíon Nefrológica, Departamento de Fisiología y Farmacología, Universidad de Salamanca, Spain.
Cell Signal. 1997 Jan;9(1):59-63. doi: 10.1016/s0898-6568(96)00091-5.
This study investigates the proliferative effect of adenosine (ADO) in cultured mesangial cells, and the possible mediation of A1 and/or A2 receptors in this proliferative effect of ADO. ADO (10(-5) M) induced a significant increase in the [3H]thymidine incorporation into DNA with respect to quiescent cells. This increase was similar to that obtained with the ADO A1 receptor agonist, R-PIA (10(-5) M), and with the ADO A2 receptor agonist, NECA (10(-5) M). Theophylline (10(-4) M), and ADO receptors inhibitor, completely inhibits the ADO-induced proliferation. The combinations NECA + A2 receptor antagonist, PD 116,948 (AT1, 10(-6) M) and PIA + A2 receptor antagonists, PD 115,199 (AT2, 10(-2) M) did not induce any significant difference with respect to cells maintained in control conditions. These findings demonstrate the proliferative effect of ADO in cultured mesangial cells, and that this effect is not specific to either of A1 or A2 receptors activation.
本研究探讨了腺苷（ADO）对培养的系膜细胞的增殖作用，以及A1和/或A2受体在ADO这种增殖作用中可能的介导作用。与静止细胞相比，ADO（10⁻⁵ M）使[³H]胸腺嘧啶核苷掺入DNA的量显著增加。这种增加与使用ADO A1受体激动剂R-PIA（10⁻⁵ M）和ADO A2受体激动剂NECA（10⁻⁵ M）所获得的增加相似。茶碱（10⁻⁴ M），一种ADO受体抑制剂，完全抑制了ADO诱导的增殖。NECA与A2受体拮抗剂PD 116,948（AT1，10⁻⁶ M）以及PIA与A2受体拮抗剂PD 115,199（AT2，10⁻² M）的组合，与处于对照条件下的细胞相比，未诱导出任何显著差异。这些发现证明了ADO对培养的系膜细胞具有增殖作用，并且这种作用并非特异性地由A1或A2受体激活所介导。
