Cigarette smoke extract decreases human bone marrow mesenchymal stromal cell adipogenic differentiation

Smoking and nicotine impose detrimental health effects including adipose tissue dysfunction. Despite extensive physiological evidence, the cellular mechanisms remain poorly understood, with few studies examining the effects of cigarette smoke extract (CSE) or nicotine on adipocyte differentiation. Primary human bone marrow-derived mesenchymal stromal cells (MSCs) were exposed to CSE or nicotine (50–500 ng/ml) during adipogenic differentiation. Cell viability and metabolic activity were assessed via MTT assay. Lipid droplet accumulation was evaluated using Sudan III staining and quantitative image analysis. Adiponectin, IL6, and IL8 concentrations were measured after 35 days using ELISA. At these doses, CSE and nicotine do not immediately affect cell viability but inhibit undifferentiated cell proliferation. Notably, both agents at 50 ng/ml significantly increased lipid accumulation during adipogenesis, while higher CSE doses nearly completely inhibited this process. Additionally, CSE dose-dependently decreased adiponectin secretion and increased IL6 and IL8, indicating a shift towards an inflammatory state. Nicotine alone primarily increased IL6 secretion with less pronounced effects. The study highlights the complex impact of CSE and nicotine on adipocyte function during early differentiation from MSCs. Dose-dependent changes in lipid accumulation, cytokine, and adiponectin secretion induced by CSE and nicotine can partly explain smoking-related adipose tissue dysfunction. • Cigarette smoke extract exposure dose-dependently impairs the lipid accumulation during MSC adipogenesis. • Cigarette smoke extract exposure leads to frustrated adipogenesis. • Cigarette smoke extract exposure shifts the secretory profile by increasing IL6 and IL8 and decreasing adiponectin secretion. • The effect of nicotine alone does not explain the observed results.