Brodnanova Maria, Cibulka Michal, Grendar Marian, Gondas Eduard, Kolisek Martin
Biomedical Centre Martin, Jessenius Faculty of Medicine in Martin, Comenius University Bratislava, 03601 Martin, Slovakia.
Department of Pharmacology, Jessenius Faculty of Medicine in Martin, Comenius University Bratislava, 03601 Martin, Slovakia.
Int J Mol Sci. 2024 Dec 11;25(24):13274. doi: 10.3390/ijms252413274.
Together with chronic inflammation, disturbed magnesium homeostasis is a factor accompanying chronic disease which thus contributes to a reduced quality of human life. In this study, our objective was to examine the possible IL-6-mediated chronic inflammation-dependent regulation of nine magnesiotropic genes encoding for constituents of magnesium homeostasis of the cell. We used three cell lines (HepG2, U-266, and PANC-1), all characterized by high expression of the gene and the presence of a membrane form of IL-6R capable of responding to human IL-6. Despite the confirmed activation of the IL-6R/JAK/STAT3 pathway after hIL-6 treatment, we observed no biologically relevant changes in the transcription intensity of the studied magnesiotropic genes. This, however, does not exclude the possibility that IL-6 can affect magnesium homeostasis at levels other than through modified transcription.
与慢性炎症一起,镁稳态紊乱是伴随慢性疾病的一个因素,从而导致人类生活质量下降。在本研究中,我们的目的是研究白细胞介素-6(IL-6)介导的慢性炎症依赖性对九个编码细胞镁稳态成分的镁转运基因的调控作用。我们使用了三种细胞系(HepG2、U-266和PANC-1),所有细胞系均具有该基因高表达以及存在能够对人IL-6作出反应的膜形式IL-6受体的特征。尽管在人IL-6处理后证实了IL-6受体/Janus激酶/信号转导和转录激活因子3(IL-6R/JAK/STAT3)途径的激活,但我们未观察到所研究的镁转运基因转录强度有生物学相关变化。然而,这并不排除IL-6可以通过转录修饰以外的水平影响镁稳态的可能性。