Apoptotic endometrial caspase-3 mediated phospholipase a2 activation, a critical component in programing uterine receptivity.

BioRxiv : the Preprint Server for Biology
S. GarvinP. Jeyasuria

Abstract

The objective of this study was to determine the consequence of uterine apoptotic caspase-3 activation on day 1 post coitus (dpc) in the pregnant mouse. We previously demonstrated that during pregnancy uterine caspase-3 activation isolated to the myometrial compartment is largely non-apoptotic and controls uterine quiescence. In this study we determined that uterine caspase-3 activation on 1 dpc may play a critical role in regulating endometrial PGE2 synthesis though iPLA2 activation. These analyses provide novel insight into the molecular mechanisms that regulate previously reported increases in endometrial PGE2 synthesis in very early pregnancy, that act to enhance uterine receptivity. We have identified the site and impact of that uterine apoptotic caspase-3 activation utilizing uteri isolated from non-pregnant control animals at estrous and diestrous and from control pregnant mice at 1-19 dpc. In addition, uteri were isolated from non-ligated controls (GD), unilateral (UL) and bilateral ligated (BL) uterine horn mouse models at 1, 3 and 6 dpc. Uteri were examined for apoptotic indices, such as caspase-3 activation and TUNEL staining. Immunohistochemical analysis was performed to identify the site of apoptotic caspase-3 act...Continue Reading

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