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Gentamicin activates rat mesangial cells. A role for platelet activating factor
A Rodriguez-Barbero1, A M Rodriguez-Lopez, R Gonzalez-Sarmiento
1Instituto Reina Sofia de Investigaciones Nefrológicas, Departamento de Fisiología y Farmacología, Facultad de Medicina, Universidad de Salamanca, Spain.
Kidney International
|May 1, 1995
Summary
Gentamicin harms kidney function by activating mesangial cells. This effect is mediated by platelet-activating factor (PAF) synthesis and release, which can be blocked by PAF antagonists.
Area of Science:
- Nephrology
- Cell Biology
- Pharmacology
Background:
- Gentamicin can decrease glomerular filtration rate.
- This decline may involve mesangial cell contraction or vasoactive hormones.
- Platelet-activating factor (PAF) is a potential mediator.
Purpose of the Study:
- To investigate gentamicin's effects on mesangial cell proliferation, contraction, and calcium mobilization.
- To assess the role of PAF in gentamicin-induced mesangial cell activation.
Main Methods:
- Cultured rat mesangial cells were treated with gentamicin.
- Effects on cell surface area, intracellular calcium ([Ca2+]i), and DNA synthesis ([3H]thymidine incorporation) were measured.
- PAF synthesis, release, and c-fos mRNA expression were assessed.
- PAF receptor antagonists (BN-52021, alprazolam, BB-823) were used to block effects.
Main Results:
- Gentamicin reduced mesangial cell surface area, increased [Ca2+]i, and stimulated DNA synthesis.
- These effects were blunted or inhibited by PAF antagonists.
- Gentamicin induced c-fos mRNA expression and stimulated PAF synthesis and release from mesangial cells.
Conclusions:
- Gentamicin activates mesangial cell functions, including proliferation and contraction.
- Platelet-activating factor (PAF) plays a significant role in mediating gentamicin's effects on mesangial cells.
- Targeting PAF may offer a therapeutic strategy to mitigate gentamicin-induced kidney damage.