Liang R F
Department of Dental Pharmacology, Meikai University School of Dentistry, Saitama, Japan.
Meikai Daigaku Shigaku Zasshi. 1990;19(1):1-20.
Effects of transforming growth factor (TGF)-beta, epidermal growth factor (EGF), insulin, 1, 25-dihydroxyvitamin D3 (1, 25 (OH)2D3), and parathyroid hormone (PTH) on the proliferation and differentiation of clonal dental pulp cells of rats were investigated. Interaction between growth factors (TGF-beta and EGF) and two hormones insulin and 1, 25 (OH)2D3, which have been noticed to accelerate the differentiation of the cells, were also studied, and the following results were obtained: 1) TGF-beta decreased alkaline phosphatase (ALPase) activity in a dose-dependent manner, and the inhibitory effect was not blocked by indomethacin, suggesting that the effect of TGF-beta on the cells may not be mediated by prostaglandins. Inhibitory effects of ALPase antagonists (L-phenylalanine, L-homoarginine, levamisole) on the activity were not affected by TGF-beta. TGF-beta showed no evident effect on the DNA synthesis (incorporation of [3H] thymidine) and collagen synthesis (incorporation of [2, 3-3H] proline into the collagenase-digestible protein) of the cells. 2) EGF stimulated the incorporation of [3H] thymidine and inhibited the ALPase activity. The inhibitory effect was not blocked by indomethacin, indicating that the EGF effect is not mediated by prostaglandins. Collagen synthesis was significantly inhibited by EGF. 3) Insulin showed a weak but significant inhibition of the DNA synthesis. Insulin increased the ALPase activity evidently, and accelerated the collagen synthesis significantly. 4) The vitamin 1, 25 (OH)2D3 significantly increased the ALPase activity though no significant changes were observed in the DNA synthesis and collagen synthesis. 5) PTH had no evident effect on the DNA synthesis and ALPase activity, but did tend to accelerate the collagen synthesis. 6) A study on the interaction between insulin and EGF or TGF-beta revealed that the acceleration of DNA synthesis induced by EGF was inhibited when the factor was combined with insulin, and the increase in ALPase activity elicited by insulin was inhibited by EGF and weakened by TGF-beta significantly when these factors were added simultaneously with the insulin. Or viewed another way, the inhibitory effect of EGF or TGF-beta on the ALPase activity was antagonized by insulin. The accelerative action of insulin on collagen synthesis was antagonized by EGF and potentiated by TGF-beta. 7) A study on the interaction between 1, 25 (OH)2D3 and EGF or TGF-beta revealed that 1, 25 (OH)2D3 inhibited the accelerating effect of EGF on the DNA synthesis and that the increasing effect of 1, 25 (OH)2D3 on ALPase activity was strongly inhibited by EGF.(ABSTRACT TRUNCATED AT 400 WORDS)
研究了转化生长因子（TGF）-β、表皮生长因子（EGF）、胰岛素、1,25-二羟基维生素D3（1,25(OH)2D3）和甲状旁腺激素（PTH）对大鼠克隆牙髓细胞增殖和分化的影响。还研究了生长因子（TGF-β和EGF）与两种已被注意到可加速细胞分化的激素胰岛素和1,25(OH)2D3之间的相互作用，得到以下结果：1）TGF-β以剂量依赖方式降低碱性磷酸酶（ALPase）活性，且吲哚美辛不能阻断这种抑制作用，提示TGF-β对细胞的作用可能不是由前列腺素介导的。ALPase拮抗剂（L-苯丙氨酸、L-高精氨酸、左旋咪唑）对该活性的抑制作用不受TGF-β影响。TGF-β对细胞的DNA合成（[3H]胸腺嘧啶掺入）和胶原合成（[2,3-3H]脯氨酸掺入胶原酶可消化蛋白）无明显影响。2）EGF刺激[3H]胸腺嘧啶掺入并抑制ALPase活性。吲哚美辛不能阻断这种抑制作用，表明EGF的作用不是由前列腺素介导的。EGF显著抑制胶原合成。3）胰岛素对DNA合成有微弱但显著的抑制作用。胰岛素明显增加ALPase活性，并显著加速胶原合成。4）维生素1,25(OH)2D3显著增加ALPase活性，而DNA合成和胶原合成未见明显变化。5）PTH对DNA合成和ALPase活性无明显影响，但有加速胶原合成的趋势。6）胰岛素与EGF或TGF-β相互作用的研究表明，EGF与胰岛素联合时，其诱导的DNA合成加速受到抑制，胰岛素诱导的ALPase活性增加在EGF存在时受到抑制，当这些因子与胰岛素同时添加时，TGF-β使其明显减弱。或者换个角度看，EGF或TGF-β对ALPase活性的抑制作用被胰岛素拮抗。胰岛素对胶原合成的促进作用被EGF拮抗，被TGF-β增强。7）1,25(OH)2D3与EGF或TGF-β相互作用的研究表明，1,25(OH)2D3抑制EGF对DNA合成的促进作用，且EGF强烈抑制1,25(OH)2D3对ALPase活性的增加作用。（摘要截短至400字）
