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Hemin-induced Erk1/2 activation and heme oxygenase-1 expression in human umbilical vein endothelial cells.

机译:血红素诱导人脐静脉内皮细胞中的Erk1 / 2活化和血红素加氧酶-1表达。

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摘要

Hemin has been reported to be protective in the pathological process, but its protective mechanisms have not been precisely defined. Hemin could induce Erk1/2 phosphorylation in astrocyte. Erk1/2 phosphorylation has been proved to be involved in many growth signals cellular transduction. However, little study has been conducted as to the relationship between hemin and Erk1/2 activation in human umbilical vein endothelial cells (HUVECs). The present study aimed to investigate the relationship between hemin and Erk1/2 phosphorylation in HUVECs. The results showed that low concentration of hemin induced and sustained phosphorylation of Erk1/2 for a long time. The HO inhibitor protoporphyrin IX zinc (II) abrogated phosphorylation of Erk1/2 induced by hemin. Biliverdin, one of the metabolites of hemin, obviously induced the Erk1/2 phosphorylation in HUVECs. Both hemin and biliverdin promoted HUVEC cell growth. The results strongly suggested that hemin could induce and sustain Erk1/2 phosphorylation in HUVECs by way of HO-1 induction and biliverdin produced from HO-1 catalysing hemin degradation.
机译:据报道,血红素在病理过程中具有保护作用,但其保护机制尚未明确。血红素可诱导星形胶质细胞中Erk1 / 2磷酸化。已证明Erk1 / 2磷酸化参与许多生长信号的细胞转导。然而,关于人脐静脉内皮细胞(HUVEC)中的血红素和Erk1 / 2活化之间的关系的研究很少。本研究旨在探讨HUVEC中血红素与Erk1 / 2磷酸化之间的关系。结果表明,低浓度的血红素可长时间诱导并持续使Erk1 / 2磷酸化。 HO抑制剂原卟啉IX锌(II)消除了血红素诱导的Erk1 / 2的磷酸化。 Biliverdin是血红素的一种代谢产物,明显诱导了HUVEC中Erk1 / 2的磷酸化。血红素和biliverdin都促进HUVEC细胞生长。结果强烈表明,血红素可以通过HO-1诱导和HO-1产生的联肝素催化血红素的降解而诱导并维持HUVECs中的Erk1 / 2磷酸化。

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