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 IL6R 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.
Keywords: SLC41A1; STAT3; inflammation; interleukin-6; magnesium.