Selol (Se IV) modulates adhesive molecules in control and TNF-α-stimulated HMEC-1 cells

• Published in: Journal of trace elements in medicine and biology Vol. 51; pp. 106 - 114
• Main Authors: Grosicka-Maciąg, Emilia, Kurpios-Piec, Dagmara, Woźniak, Katarzyna, Kowalewski, Cezary, Szumiło, Maria, Drela, Nadzieja, Kiernozek, Ewelina, Suchocki, Piotr, Rahden-Staroń, Iwonna
• Format: Journal Article
• Language: English
• Published: Germany Elsevier GmbH 01.01.2019
• Subjects: Adhesion molecules; Cell Adhesion Molecules - biosynthesis; Cell Proliferation - drug effects; Cell Survival - drug effects; Cells, Cultured; Dose-Response Relationship, Drug; Endothelial Cells - drug effects; Endothelial Cells - metabolism; Humans; Inflammation - drug therapy; Inflammation - metabolism; Molecular Structure; NF-B; Reactive oxygen species; Selenium Compounds - chemistry; Selenium Compounds - pharmacology; Selol; Structure-Activity Relationship; TNF-α; Tumor Necrosis Factor-alpha - metabolism; Adhesion molecules; NF-B; Reactive oxygen species; TNF-α; Selol
• ISSN: 0946-672X; 1878-3252
• DOI: 10.1016/j.jtemb.2018.10.005

[Display omitted] •Selol in HMEC-1 cells shows a pro-inflammatory activity in parallel with effects on CAMs expression on the cell surface.•Selol in HMEC-1 cells activates NF-κB.•Selol in HMEC-1 cells downregules PECAM-1, VCAM-1 and upregulates ICAM-1 expression on cell surface of control cells.•Selol in HMEC-1 cells enhances ICAM-1 and VCAM-1 expression level when is present concomitantly with TNF-α. Selol, an organic selenitetrigliceride formulation containing selenium at +4 oxidation level, has been suggested as anticancer drug. One of the causes of several diseases including cancer may be inflammation. This study aimed at determining the activity of Selol via measuring its effect on reactive oxygen species (ROS) generation, nuclear factor kappa B (NF-κB) activation, intercellular cell adhesion molecules-1 (ICAM-1), vascular cell adhesive molecule-1 (VCAM-1), and plateled-endothelial cell adhesive molecule-1 (PECAM-1) levels on control and on tumor necrosis factor-α (TNF-α)-stimulated human microvascular endothelial cells (HMEC-1). Cells were treated either with Selol 5% (4 or 8 μgSe/mL) or TNF-α (10 ng/mL) alone or with Selol concomitant with TNF-α. Selol treatment resulted in ROS generation, activation of NF-κB, downregulation of PECAM-1, VCAM-1 and slight upregulation ICAM-1 expression on the cell surface. TNF-α treatment reflected in sharp NF-κB activation, upregulation of both ICAM-1 and VCAM-1 in parallel with the downregulation of PECAM-1 expression on cell surface. Exposure to both compounds upregulated ICAM-1 and VCAM-1, downregulated PECAM-1 level on cell surface in parallel with no changes in level of NF-κB activation as compared with effects mediated by TNF-α alone. These results points to new look at Selol action since it shows a pro-inflammatory activity in parallel with effects on CAMs expression on the cell surface of human microvascular endothelial cells. However, since Selol enhances CAMs expression level when is present concomitantly with TNF-α this fact might suggest that selenium present in the condition of inflammation will make it worse.