ArticlePhysiological reports2025
Medin induces pro-inflammatory activation of human brain vascular smooth muscle cells.
Article in Physiological reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Neutrophils and aortic medial amyloid: mutually beneficial or a dangerous combination?Frontiers in immunology · 2026Article
- Aortic Stiffness and Alzheimer's Disease: The Medin Connection.Biomolecules · 2025Review
- Medin induces pro-inflammatory activation of human brain vascular smooth muscle cells.Physiological reports · 2025Article
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6 authors.
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Abstract
Medin, a common amyloidogenic protein, accumulates in the vasculature with aging. We evaluated the effects of medin on human brain vascular smooth muscle cell (VSMC) activation. VSMCs were exposed to medin (0.5, 1, and 5 μM) without or with the small molecule nuclear factor-κB (NFκB) inhibitor RO106-9920 (10 μM). Polymerase chain reaction, Western blot/enzyme-linked immunosorbent assays were used to quantify gene and protein expressions/secretions, respectively, of pro-inflammatory factors (interleukin (IL)-6, IL-8, and monocyte chemoattractant protein (MCP)-1) and structural and enzyme proteins associated with VSMC phenotypic transformation (smooth muscle actin alpha 2 (ACTA2), myosin heavy chain 11 (MYH11) and NADPH oxidase 4 (NOX4)). Medin increased VSMC gene expression and protein secretion of IL-6, IL-8, and MCP-1 (protein secretion 46.0 ± 12.8x, 20.2 ± 4.1x, and 8.7 ± 3.1x, respectively, medin 5 μM versus vehicle, p < 0.05). There was no change in gene/protein expressions of ACTA2, MYH11, and NOX4. Co-treatment with RO106-9920 reduced medin-induced increases in IL-6 and IL-8 with a trend towards reduced MCP-1 secretion. Medin induced pro-inflammatory activation of human brain VSMCs that is mediated in part by NFκB. Acute medin treatment did not alter structural proteins involved in VSMC phenotypic transformation. The findings support medin as a potential novel mediator of and therapeutic target for vascular aging pathology.
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