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Monocyte/mesangial cell interactions in high-glucose co-cultures.
P Menè1, C Caenazzo, F Pugliese
1Department of Clinical Sciences, Division of Nephrology, University La Sapienza, Rome, Italy.
Summary
High glucose increases monocyte adhesion to human mesangial cells (HMC), altering HMC growth and extracellular matrix production. These interactions may contribute to diabetic kidney disease progression.
Area of Science:
- Nephrology
- Cell Biology
- Diabetology
Background:
- Monocyte adhesion to human mesangial cells (HMC) is implicated in diabetic glomerulopathy.
- Diabetic microenvironments may influence leukocyte-glomerular cell interactions.
- This study investigates the impact of a diabetic milieu on HMC and monocyte interactions.
Purpose of the Study:
- To examine how co-culture with U937 myelomonocytes in a high glucose environment affects HMC phenotype, growth, and extracellular matrix production.
- To understand the role of glucose levels in monocyte-HMC interactions.
Main Methods:
- Co-culture of HMC with U937 cells in normal (NG) and high glucose (HG) media.
- Assessing cell adhesion, apoptosis (TUNEL/propidium iodide), and cell morphology via image analysis.
- Analyzing gene and protein expression of urokinase-plasminogen activator (uPA), collagen type IV (COL IV), TGF-beta1, MMPs, and TIMPs using RT-PCR, zymography, and ELISA.
Main Results:
- High glucose significantly increased U937 cell adhesion to HMC.
- HG conditions promoted HMC growth and increased transcription/secretion of uPA, COL IV, and TGF-beta1.
- Monocyte adhesion reduced HMC number and altered spatial distribution, with effects diminishing by 48 hours.
Conclusions:
- High glucose enhances monocyte adhesion to HMC.
- Monocytes and glucose levels interact to modulate HMC behavior and extracellular matrix production.
- These findings suggest a mechanism contributing to mesangial expansion and glomerulosclerosis in diabetes.