Park Young-Kwon, Ahn Dae-Ro, Oh Myoungsuk, Lee Taekyoung, Yang Eun Gyeong, Son Miwon, Park Hyunsung
Department of Life Science, University of Seoul, Seoul, Korea.
Mol Pharmacol. 2008 Jul;74(1):236-45. doi: 10.1124/mol.108.045278. Epub 2008 Apr 21.
We have confirmed that the NO donor (+/-)-S-nitroso-N-acetylpenicillamine (SNAP) stabilizes the transactive form of hypoxia-inducible factor-1alpha (HIF-1alpha), leading to the induction of HIF-1alpha target genes such as vascular endothelial growth factor and carbonic anhydrase 9. Activation of HIF-1alpha should require inhibition of the dual system that keeps it inactive. One is ubiquitination, which is triggered by hydroxylation of HIF-1alpha-proline and the subsequent binding of E3 ubiquitin ligase, the von Hippel Lindau (VHL) protein. The other is hydroxylation of HIF-1alpha-asparagine, which reduces the affinity of HIF-1alpha for its coactivator, cAMP responsive element binding protein/p300. We examined the effects of the NO donor SNAP on proline and asparagine hydroxylation of HIF-1alpha peptides by measuring the activities of the corresponding enzymes, HIF-1alpha-specific proline hydroxylase 2 (PHD2) and the HIF-1alpha-specific asparagine hydroxylase, designated factor inhibiting HIF-1alpha (FIH-1), respectively. We found that the SNAP did not prevent PHD2 from hydroxylating the proline of HIF-1alpha. Instead, it blocked the interaction between VHL and the proline-hydroxylated HIF-1alpha, but only when the reducing agents Fe(II) and vitamin C were limiting. The fact that the absence of cysteine 520 of HIF-1alpha abolishes its responsiveness to SNAP suggests that this residue mediates the inhibition by SNAP of the interaction between VHL and HIF-1alpha, presumably by S-nitrosylation of HIF-1alpha. Un-like PHD2, asparagine hydroxylation by FIH-1 was directly inhibited by SNAP, but again only when reducing agents were limiting. Substitution of cysteine 800 of HIF-1alpha with alanine failed to reverse the inhibitory effects of SNAP on asparagine hydroxylation, implying that FIH-1, not its substrate HIF-1alpha, is inhibited by SNAP.
我们已证实,一氧化氮供体(±)-S-亚硝基-N-乙酰青霉胺(SNAP)可稳定缺氧诱导因子-1α(HIF-1α)的反式激活形式,从而导致HIF-1α靶基因如血管内皮生长因子和碳酸酐酶9的诱导。HIF-1α的激活应需要抑制使其保持无活性的双重系统。一个是泛素化,它由HIF-1α-脯氨酸的羟基化以及随后E3泛素连接酶即冯·希佩尔·林道(VHL)蛋白的结合引发。另一个是HIF-1α-天冬酰胺的羟基化,它降低了HIF-1α对其共激活因子cAMP反应元件结合蛋白/p300的亲和力。我们通过分别测量相应酶即HIF-1α特异性脯氨酸羟化酶2(PHD2)和HIF-1α特异性天冬酰胺羟化酶(称为HIF-1α抑制因子,FIH-1)的活性,研究了一氧化氮供体SNAP对HIF-1α肽脯氨酸和天冬酰胺羟基化的影响。我们发现SNAP并不能阻止PHD2对HIF-1α脯氨酸的羟基化。相反,它阻断了VHL与脯氨酸羟基化的HIF-1α之间的相互作用,但仅在还原剂亚铁离子(Fe(II))和维生素C有限时才会如此。HIF-1α的半胱氨酸520缺失消除其对SNAP的反应性这一事实表明,该残基介导了SNAP对VHL与HIF-1α之间相互作用的抑制,推测是通过HIF-1α的S-亚硝基化实现的。与PHD2不同,FIH-1对天冬酰胺的羟基化直接受到SNAP的抑制,但同样仅在还原剂有限时才会如此。将HIF-1α的半胱氨酸800替换为丙氨酸未能逆转SNAP对天冬酰胺羟基化的抑制作用,这意味着受SNAP抑制的是FIH-1,而非其底物HIF-1α。