Related Experiment Video
Updated: Jun 11, 2025
Dual Effects of Melanoma Cell-derived Factors on Bone Marrow Adipocytes Differentiation
Published on: August 23, 2018
Cigarette smoke extract decreases human bone marrow mesenchymal stromal cell adipogenic differentiation
Janne Heikkinen1, Sanna Palosaari2, Petri Lehenkari3
1Medical Faculty, Translational Medicine Research Unit, University of Oulu, Oulu, Finland.
Background:
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.
Methods:
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.
Results:
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.
Conclusion:
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.
Insights
Cigarette smoke extract (CSE) and nicotine impact early adipocyte differentiation. Low doses increase lipid accumulation, while higher doses and CSE promote inflammation, contributing to smoking-related adipose tissue dysfunction.
Area of Science:
- Cell biology
- Metabolic research
- Toxicology
Background:
- Smoking and nicotine cause adipose tissue dysfunction.
- Cellular mechanisms underlying these effects are not well understood.
- Limited research exists on cigarette smoke extract (CSE) and nicotine's impact on adipocyte differentiation.
Purpose of the Study:
- To investigate the effects of CSE and nicotine on adipocyte differentiation.
- To elucidate cellular mechanisms of smoking-related adipose tissue dysfunction.
Main Methods:
- Human bone marrow-derived mesenchymal stromal cells (MSCs) were differentiated into adipocytes with CSE or nicotine exposure.
- Cell viability, metabolic activity, and lipid accumulation were assessed.
- Adiponectin, IL6, and IL8 secretion levels were measured.
Main Results:
- CSE and nicotine did not affect cell viability but inhibited proliferation.
- Low-dose CSE/nicotine (50 ng/ml) increased lipid accumulation; higher CSE doses inhibited it.
- CSE decreased adiponectin and increased IL6/IL8, indicating inflammation; nicotine primarily increased IL6.
Conclusions:
- CSE and nicotine have complex, dose-dependent effects on adipocyte differentiation.
- Altered lipid accumulation and cytokine profiles contribute to smoking-related adipose tissue dysfunction.
More Related Videos
08:40Optimization of the Wound Scratch Assay to Detect Changes in Murine Mesenchymal Stromal Cell Migration After Damage by Soluble Cigarette Smoke Extract
Published on: December 3, 2015
11:00Isolation and Enrichment of Human Adipose-derived Stromal Cells for Enhanced Osteogenesis
Published on: January 12, 2015