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Adenosine activates mesangial cell proliferation
M MacLaughlin1, C Martinez-Salgado, N Eleno
1Instituto Reina Sofía de Investigacíon Nefrológica, Departamento de Fisiología y Farmacología, Universidad de Salamanca, Spain.
Abstract:
This study investigates the proliferative effect of adenosine (ADO) in cultured mesangial cells, and the possible mediation of A1 and/or A2 receptors in this proliferative effect of ADO. ADO (10(-5) M) induced a significant increase in the [3H]thymidine incorporation into DNA with respect to quiescent cells. This increase was similar to that obtained with the ADO A1 receptor agonist, R-PIA (10(-5) M), and with the ADO A2 receptor agonist, NECA (10(-5) M). Theophylline (10(-4) M), and ADO receptors inhibitor, completely inhibits the ADO-induced proliferation. The combinations NECA + A2 receptor antagonist, PD 116,948 (AT1, 10(-6) M) and PIA + A2 receptor antagonists, PD 115,199 (AT2, 10(-2) M) did not induce any significant difference with respect to cells maintained in control conditions. These findings demonstrate the proliferative effect of ADO in cultured mesangial cells, and that this effect is not specific to either of A1 or A2 receptors activation.
Insights
Adenosine (ADO) stimulates proliferation in cultured mesangial cells. This effect is mediated by ADO receptors but is not specific to either A1 or A2 subtypes.
Area of Science:
- Nephrology
- Cell Biology
- Pharmacology
Background:
- Adenosine (ADO) is a nucleoside with diverse physiological roles.
- Mesangial cells are crucial components of the kidney glomerulus.
- The role of adenosine receptors in mesangial cell proliferation requires further elucidation.
Purpose of the Study:
- To investigate the proliferative effect of adenosine on cultured mesangial cells.
- To determine the involvement of A1 and A2 adenosine receptors in this proliferative response.
Main Methods:
- Cultured human mesangial cells were treated with adenosine (ADO) and specific receptor agonists/antagonists.
- [3H]thymidine incorporation was measured to assess DNA synthesis and cellular proliferation.
- Theophylline, an ADO receptor inhibitor, was used to block ADO-induced proliferation.
Main Results:
- Adenosine (10(-5) M) significantly increased [3H]thymidine incorporation in mesangial cells.
- Both A1 and A2 receptor agonists (R-PIA and NECA, respectively) mimicked this proliferative effect.
- Theophylline completely inhibited adenosine-induced proliferation, confirming receptor mediation.
- Combinations of agonists with specific antagonists did not reveal a subtype-specific effect.
Conclusions:
- Adenosine exerts a proliferative effect on cultured mesangial cells.
- This proliferative effect is mediated through adenosine receptors.
- The study suggests that neither A1 nor A2 receptor activation is solely responsible for adenosine-induced mesangial cell proliferation.