Fig. 5: Endogenous preconditioning facilitates the maintenance of non-apoptotic CASP3 and suppresses iPLA2 activation in the pregnant mouse uterus. | Cell Death & Disease

Fig. 5: Endogenous preconditioning facilitates the maintenance of non-apoptotic CASP3 and suppresses iPLA2 activation in the pregnant mouse uterus.

From: Preconditioning the uterine unfolded protein response maintains non-apoptotic Caspase 3-dependent quiescence during pregnancy

Fig. 5

Uteri collected from vehicle treated (Con), sub-preconditioned (PBA), exogenously stressed-sub-preconditioned (TM+PBA) and exogenously stressed-preconditioned (TM) mice on E17 prior to the onset of preterm and term birth were examined for a active Cl CASP3. b Cl PARP, and c TUNEL staining to measure apoptotic cell death. iPLA2t levels act as an indirect measure of iPLA2 activation (d). Cl CASP3 levels remained unchanged across all 4 groups examined however increased Cl PARP and TUNEL activity and decreased levels of the inactive iPLA2t were isolated to the TM+PBA-treated mice. e In the hTERT-HM cells the cleaved active monomeric form of iPLA2 (iPLA2cm) was elevated in a relative manner to the levels of apoptotic CASP3 present in the preconditioned and non-preconditioned cells (Fig. 1a). A representative blot or image from each experiment is shown. PDIA2 and NCOA3 are utilized as cytoplasmic and nuclear protein loading controls. Statistical comparisons were performed using one-way ANOVA, and subsequent Newman–Keuls multiple-comparison tests. Data labeled with different letters are significantly different from each other (p < 0.05)

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