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首页> 外文期刊>American Journal of Physiology >Letter to the editor: Is homocysteine the culprit molecule in vascular diseases or just a bystander?
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Letter to the editor: Is homocysteine the culprit molecule in vascular diseases or just a bystander?

机译:致编辑的信:是血管疾病中的罪魁祸首分子或只是一个旁观者吗?

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to the editor: Jiang et al. (3) reported an important finding that vascular smooth cell migration was promoted by the resistin gene expression induced by ultrahigh concentrations of homo-cysteine (500 muM). The homocysteine concentrations used by Jiang et al. were markedly higher than the physiological concentrations (<100 muM); therefore, the biological significance of the results of their study should be interpreted with caution. Since supraphysiological concentrations of homocysteine are required to induce resistin expression, the role of homocysteine in vascular cell migration is debatable. To assess the effects of homocysteine at physiological levels, Wang et al. (5) developed a method in which erythro-9 (2-hydroxy-3-nonyl)-adenine hydrochloride (EHNA) and adenosine were added to homocysteine to convert homocysteine into its more toxic form S-adenosylhomocysteine (SAH). This protocol has been used in many studies to study the effects of homocysteine on gene expression.
机译:向编辑:江等人。 (3)报道了一种重要的发现,血管光滑细胞迁移通过超高浓度的同源半胱氨酸(500mum)诱导的抗毒素基因表达促进。 江等人使用的同型半胱氨酸浓度。 明显高于生理浓度(<100毫米); 因此,应谨慎地解释他们研究结果的生物学意义。 由于异证浓度的致力学浓度是诱导抵抗素的表达,因此同型半胱氨酸在血管细胞迁移中的作用是难题的。 王等人来评估同型半胱氨酸的影响,Wang等人。 (5)制定了一种方法,其中将红霉-9(2-羟基-3-壬基) - 盐酸盐(EHNA)和腺苷加入到同型半胱氨酸中以将同型半胱氨酸转化为其更具毒性形式的S-腺囊肌细胞(SAH)。 该方案已被用于许多研究中,以研究同型半胱氨酸对基因表达的影响。

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