IQUIFIB   02644
INSTITUTO DE QUIMICA Y FISICOQUIMICA BIOLOGICAS "PROF. ALEJANDRO C. PALADINI"
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
Molecular mechanisms involved in COX-2 expression under hypertonic stress.
Autor/es:
CASALI, CECILIA IRENE; WEBER, KAREN; FAGGIONATO, DANIELA; GOMEZ MOREL, EMANUEL; FERNANDEZ TOME, MARIA DEL CARMEN
Lugar:
San Luis
Reunión:
Congreso; SAIB; 2011
Resumen:
Renal medullary cells are exposed to variable and high concentrations of NaCl as part of the urinary concentrating system. Despite such adverse conditions, renal cells still survive and function by activating the transcription of various osmoprotective genes, among them, cyclooxygenase 2 (COX2). It was reported that PI3K and ERK1/2 are signaling pathways involved in cell survival and activated by osmotic stress. Therefore, in the present work we studied their role in the induction of COX2 expression reported as cytoprotective protein. With this purpose cultures of the renal cell line MDCK were grown during 5, 15, 30, 60 min and 1.5, 3, 6, 12 and 24 h in isotonic (298 mOsm/Kg H2O) and NaCl-hypertonic (500 mOsm/Kg H2O), in the absence or presence of different specific inhibitors (LY294002, U0126). After the treatments cells were collected and submitted to westernblot for COX2 analysis. Hypertonic medium induced COX2 expression after 12 h of NaCl treatment. Surprisingly, LY294002, a PI3K inhibitor, did not prevent NaCl-induced COX2 expression but caused an over-expression of the protein from 6 h of treatment.  ERK1/2 inhibitor U0126 did not affect COX2 protein in 60 min of treatment but a slight decrease in COX2 was observed in long-term treatment. Our data show that PI3K and ERK1/2 signaling pathways counterbalance NaCl-induced COX2 expression contributing to renal cell survival.