Lack of TNFRp55 modifies circadian rhythms in the ovary in diestrus

DE LA VEGA M; RAGUSA JA; ARIAS JL; PONCE IT; ANZULOVICH AC; DIGENARO S; CASAIS M

Congreso; Sociedad de Biología de Cuyo XXX Reunión Científica Anual. San Luis; 2012

LACK OF TNFRp55 MODIFIES CIRCADIAN RHYTHMS IN THE OVARY IN DIESTRUS. De la Vega M, Ragusa JA, Arias JL, Ponce IT, Anzulovich AC, DiGenaro S and Casais M. PIP2399, LABIR-UNSL IMIBIO-SL, CCT-CONICET San Luis. Previously, we demonstrated that progesterone and the mRNA of its synthetic enzyme, 3β-HSD, display circadian rhythmicity in the ovary. Clock, Cry1 and Per1 are key components of the cellular clock and TNF is a cytokine that can act as a circadian modulator. Our aim was to investigate whether also 3β-HSD protein and Star mRNA present circadian variation in the ovary and whether the absence of the TNFp55 receptor affects the temporal expression of Per1, Clock and Cry1 genes, StAR mRNA and 3β-HSD protein. Wild type and TNFRp55-/- mice, were maintained on a 12h light: 12h dark cycle, at 24±2°C, with food and water ad libitum. Five days before the experiment, mice were kept under constant darkness conditions. Ovaries were isolated every 6h during a 24h period. StAR, Clock, Per1 and Cry transcripts levels were determined by RT-PCR and 3β-HSD protein was measured by western blot. As expected, Per1 and Cry1 genes expression as well as 3β-HSD protein levels display a circadian oscillation in the ovary. We did not observed circadian rhythms of Clock and StAR expression in this tissue. TNFRp55 deficiency modifies the temporal expression of Clock genes Per1 and Cry1 as well as the mesor of 3β-HSD protein rhythm. The TNFRp55-might mediate the modulation of Clock genes expression and thus the circadian regulation of the 3β-HSD expression and progesterone 24h-oscillation in the ovary in diestrus.