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Gentamicin treatment induces simultaneous mesangial proliferation and apoptosis in rats
Carlos Martínez-Salgado1, Nélida Eleno, Ana I Morales
1Departamento de Fisiología y Farmacología, Instituto Reina Sofía de Investigación Nefrológica, Universidad de Salamanca, Salamanca, Spain.
Background:
Gentamicin (G)-induced acute renal failure is characterized by an impairment of glomerular function without apparent changes in glomerular structure. However, G stimulates reactive oxygen species (ROS)-mediated mesangial cell proliferation in vitro. We studied whether G promotes mesangial cell apoptosis in vitro, and if apoptosis and proliferation in parallel may occur in glomerular cells in vivo after a renal damage induced by G treatment.
Methods:
For in vivo studies, rats were treated with G (100 mg/kg body weight/day) for 6 days, and functional and histologic studies were performed. For in vitro studies, mesangial cell proliferation and apoptosis were evaluated after 24, 48, and 72 hours of 10(-5) mol/L G incubation.
Results:
After G injections, the number of nuclei per glomerulus did not change, whereas proliferating and apoptotic cell numbers increased. G increases DNA synthesis and cell number in cultured mesangial cells, and increases markedly the apoptotic cell number. ROS scavengers superoxide dismutase and catalase reduce G-induced mesangial cell apoptosis, whereas the incubation with the ROS donor system xanthine plus xanthine oxidase increases apoptosis to levels similar to G. G-induced cellular proliferation and apoptosis either in vitro or in vivo is associated to an early increase in the pro-apoptotic protein Bax and a delayed increase in the survival protein Bcl-2.
Conclusion:
G simultaneously induces proliferation and apoptosis of mesangial cells in vitro and glomerular mesangial cells in vivo. ROS may mediate G-induced mesangial apoptosis in vitro. The equilibrium proliferation/apoptosis may maintain mesangial cell number within normal limits after a G-induced glomerular insult.
Insights
Gentamicin induces both proliferation and apoptosis in kidney mesangial cells, potentially mediated by reactive oxygen species (ROS). This balance may preserve normal cell numbers following gentamicin-induced kidney damage.
Area of Science:
- Nephrology
- Cell Biology
- Toxicology
Background:
- Gentamicin-induced acute renal failure impairs glomerular function without structural changes.
- Gentamicin stimulates reactive oxygen species (ROS)-mediated mesangial cell proliferation in vitro.
- The study investigates if gentamicin promotes mesangial cell apoptosis in vitro and if apoptosis and proliferation occur in vivo.
Purpose of the Study:
- To determine if gentamicin (G) induces apoptosis in mesangial cells in vitro.
- To investigate the in vivo occurrence of mesangial cell apoptosis and proliferation following gentamicin treatment.
- To explore the role of reactive oxygen species (ROS) in gentamicin-induced mesangial cell apoptosis.
Main Methods:
- In vivo studies involved daily gentamicin injections in rats for 6 days, followed by functional and histological assessments.
- In vitro studies evaluated mesangial cell proliferation and apoptosis after 24, 48, and 72 hours of gentamicin incubation.
- Assays included DNA synthesis, cell counting, and analysis of apoptotic and survival protein expression (Bax, Bcl-2).
Main Results:
- Gentamicin treatment in vivo increased proliferating and apoptotic cell numbers without altering the nuclei count per glomerulus.
- In vitro, gentamicin increased mesangial cell DNA synthesis, cell number, and significantly elevated apoptosis.
- Reactive oxygen species (ROS) scavengers reduced gentamicin-induced apoptosis, while ROS donors increased it, indicating ROS mediation.
Conclusions:
- Gentamicin induces simultaneous proliferation and apoptosis of mesangial cells both in vitro and in vivo.
- Reactive oxygen species (ROS) likely mediate gentamicin-induced mesangial cell apoptosis.
- The balance between proliferation and apoptosis may maintain normal mesangial cell numbers after gentamicin-induced glomerular injury.
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