Cátedra de Bioquímica Clínica II, Departamento de Biología, Bioquímica y Farmacia, Universidad Nacional del Sur, San Juan 670, B8000ICN Bahía Blanca, Argentina.
Mol Cell Endocrinol. 2011 Jun 6;339(1-2):136-43. doi: 10.1016/j.mce.2011.04.009. Epub 2011 Apr 22.
In this work we provide evidence that estrone "per se" modulates cellular endothelial growth and survival, events that play key roles in the development of vascular disease. Moreover, under oxidative stress conditions the hormone prevented apoptosis triggered by hydrogen peroxide. Although estrone did not affect E-selectin and VCAM-1 mRNAs synthesis, the hormone prevented the expression of these adhesion molecules induced by the proinflammatory agent LPS. The steroid partially attenuated leukocyte adhesion not only under basal conditions but also in the presence of LPS. Using ICI182780 compound as estrogen receptor antagonist, and PD98059 as MAPK inhibitor we obtained evidence that the mitogenic action of estrone involved the participation of ER and MAPK transduction pathway activation. The presence of estradiol impaired the effect of estrone on cell proliferation and vasoactive production. These results suggest that estrone exhibits a remarkable biological action on endothelial cells, modulating vasoactive production, proliferation, apoptosis, and cell adhesion events.
在这项工作中，我们提供了证据表明雌酮“本身”调节细胞内皮生长和存活，这些事件在血管疾病的发展中起着关键作用。此外，在氧化应激条件下，该激素可防止过氧化氢引发的细胞凋亡。尽管雌酮不影响 E-选择素和 VCAM-1mRNA 的合成，但该激素可防止由促炎剂 LPS 诱导的这些粘附分子的表达。该甾体不仅在基础条件下，而且在 LPS 存在下，部分减轻白细胞的粘附。使用 ICI182780 化合物作为雌激素受体拮抗剂，和 PD98059 作为 MAPK 抑制剂，我们获得了证据表明，雌酮的有丝分裂作用涉及 ER 和 MAPK 转导途径的激活。雌二醇的存在削弱了雌酮对细胞增殖和血管活性产物的作用。这些结果表明，雌酮对内皮细胞表现出显著的生物学作用，调节血管活性产物、增殖、凋亡和细胞粘附事件。
