Parrott D P, Lockey P M, Bright C P
Dagenham Research Centre, Rhone-Poulenc Rorer (UK) Ltd., Dagenham, Essex.
Atherosclerosis. 1991 Jun;88(2-3):213-8. doi: 10.1016/0021-9150(91)90083-f.
We have investigated the growth promoting activities of two potent vasoactive substances, serotonin and angiotensin II (AII), on cultured porcine aortic smooth muscle cells (ASMC), using a defined serum-free medium. Serotonin (30 nM to 30 microM) stimulated ASMC DNA synthesis both alone and in combination with platelet-derived growth factor (PDGF) and epidermal growth factor (EGF). Serotonin-induced DNA synthesis was significantly inhibited by ketanserin (5-hydroxytryptamine-2 (5HT-2) receptor antagonist). AII (3-10 nM) failed to stimulate ASMC DNA synthesis directly, either alone or in combination with PDGF or EGF. Since both serotonin and AII were found to activate phosphatidylinositol turnover and are reported to mobilise intracellular calcium, it is apparent that these events alone are insufficient to stimulate ASMC mitogenesis.
我们使用一种特定的无血清培养基,研究了两种强效血管活性物质——血清素和血管紧张素II(AII)对培养的猪主动脉平滑肌细胞(ASMC)的促生长活性。血清素(30 nM至30 microM)单独以及与血小板衍生生长因子(PDGF)和表皮生长因子(EGF)联合使用时,均能刺激ASMC的DNA合成。酮色林(5-羟色胺-2(5HT-2)受体拮抗剂)可显著抑制血清素诱导的DNA合成。AII(3 - 10 nM)无论是单独使用还是与PDGF或EGF联合使用,均无法直接刺激ASMC的DNA合成。由于血清素和AII均能激活磷脂酰肌醇代谢,且据报道可动员细胞内钙,显然仅这些事件不足以刺激ASMC有丝分裂。