25 research outputs found
Expression of PRB, FKBP52 and HB-EGF Relating with Ultrasonic Evaluation of Endometrial Receptivity
Background: To explore the molecular basis of the different ultrasonic patterns of the human endometrium, and the molecular marker basis of local injury. Methodology/Principal Findings: The mRNA and protein expression of FKBP52, progesterone receptor A (PRA), progesterone receptor B (PRB), and HB-EGF were detected in different patterns of the endometrium by real-time RTPCR and immunohistochemistry. There were differences in the mRNA and protein expression of FKBP52, PRB, and HB-EGF in the triple line (Pattern A) and homogeneous (Pattern C) endometrium in the window of implantation. No difference was detected in PRA expression. After local injury, the mRNA expression of HB-EGF significantly increased. In contrast, there was no difference in the mRNA expression of FKBP52, PRB, or PRA. The protein expression of FKBP52, PRB, and HB-EGF increased after local injury. There was no difference in the PRA expression after local injury. Conclusions: PRB, FKBP52, and HB-EGF may be the molecular basis for the classification of the ultrasonic patterns. HB-EGF may be the molecular basis of local injury. Ultrasonic evaluation on the day of ovulation can be effective in predicting the outcome of implantation
Gender differences in the use of cardiovascular interventions in HIV-positive persons; the D:A:D Study
Peer reviewe
Glutathione Depletion and Disruption of Intracellular Ionic Homeostasis Regulate Lymphoid Cell Apoptosis*
Intracellular glutathione (GSH) depletion is an important hallmark of
apoptosis. We have recently shown that GSH depletion by its extrusion
regulates apoptosis independently of excessive reactive oxygen species
accumulation. However, the mechanisms by which GSH depletion regulates
apoptosis are still unclear. Because disruption of intracellular ionic
homeostasis, associated with apoptotic volume decrease (AVD), is necessary for
the progression of apoptotic cell death, we sought to evaluate the
relationship between GSH transport and ionic homeostasis during Fas ligand
(FasL)-induced apoptosis in Jurkat cells. GSH depletion in response to FasL
was paralleled by distinct degrees of AVD identified by differences in
cellular forward scatter and electronic impedance analysis. Inhibition of GSH
efflux prevented AVD, K+ loss, and the activation of two distinct
ionic conductances, mediated by Kv1.3 and outward rectifying
Cl– channels. Reciprocally, stimulation of GSH loss
accelerated the loss of K+, AVD, and consequently the
progression of the execution phase of apoptosis. Although high extracellular
K+ inhibited FasL-induced apoptosis, GSH depletion was largely
independent of K+ loss. These results suggest that deregulation of
GSH and ionic homeostasis converge in the regulation of apoptosis in lymphoid
cells