N and basal plate [20]. The placenta was not examined and controlled

N and basal plate [20]. The ��-Sitosterol ��-D-glucoside web placenta was not examined and controlled sampling was not performed. Increased expression of HSP 70 was reported in placenta of what was termed “placental vascular disease” (preeclampsia, preeclampsia, preeclampsia plus IUGR all combined in one group) compared with term non-diseased placentae [21]. All were delivered by caesarean section. Labor was not studied. One study reported that HSP 70 was expressed in placenta and reported no difference between labor and non-labor however no data or p values were shown to support this statement and no systematic sampling was performed [22]. Similarly Li et al [21] found no difference between labor and non-labor but similar issues applied. Several years ago we examined HSP70 expression in placentae from normal and preeclampsia with our without IUGR [23]. Others have preformed immunofluorescence on paraffin sections. HSP 70 expression was reported to be increased in preeclampsia [24]. The presence of a uterine artery notch in a mixed group of normal pregnant, preeclampsia and preeclampsia plus IUGR was associated with increased eNOS and HSP 70 in basal plate samples taken from MedChemExpress Clavulanate (potassium) patients who underwent caesarean section. Placental villous tissue was not studied [25].Some studies have examined HSP 70 expression in early pregnancy. HSP 70 temporarily increases during 8? weeks of gestation when blood flow to the placenta is initiated leading to an oxidative stress insult [26]. HSP 70 immunostaining also increased in early pregnancy miscarriage [27]. Janiaux et al [28] examined HSP 70 and nitrotyrosine expression in placentae obtained from surgically terminated pregnancies between 8?3 weeks of gestation. They sampled the inner and outer third. Immunoreactivity for HSP 70 and nitrotyrosine residues was greater in samples from peripheral than from central regions of normal placentas and from missed miscarriages compared to controls. They proposed that oxidative damage to the trophoblast, induced by premature onset of the maternal placental circulation is a key factor in early pregnancy loss. HSP 70 was reported to be reduced in purified cytotrophoblast 1655472 cells from preeclampsia cases compared to controls however labor and site of sampling was not studied. The shock of enzyme digestion and cell purification are also confounding factors [29]. Since intracellular HSP 70 binds to the progesterone receptor and functions as a co-repressor of this receptor [30] this may in part explain our results providing a mechanism linking HSP 70 to labor. HSF-1 is the stress responsive transcriptional activator responsible for the inducible transcription of genes encoding HSPs [31]. Padmini et al [32] reported increased HSP 70 and HSF-1 in placentae from preeclampsia cases compare with uncomplicated pregnancies. Malyshev et al (1995) [33] showed that oxidative stress increases NFkB which in turn activates nitric oxide synthase, nitric oxide release and subsequently HSP 70 induction in several organs. Blocking nitric oxide synthase activity inhibited HSP 70 induction. We have previously shown that villous eNOS [34], peroxynitrite production [35] and lipid peroxidation [23] are increased in preeclampsia. HSPs can be detected in the circulation. The few reported studies of HSP 70 serum concentrations in preeclampsia and labor are conflicting [30,36]. In summary spatial changes in HSP 70 expression occur during labor and preeclampsia. The physiological and pathological significance of this remains to b.N and basal plate [20]. The placenta was not examined and controlled sampling was not performed. Increased expression of HSP 70 was reported in placenta of what was termed “placental vascular disease” (preeclampsia, preeclampsia, preeclampsia plus IUGR all combined in one group) compared with term non-diseased placentae [21]. All were delivered by caesarean section. Labor was not studied. One study reported that HSP 70 was expressed in placenta and reported no difference between labor and non-labor however no data or p values were shown to support this statement and no systematic sampling was performed [22]. Similarly Li et al [21] found no difference between labor and non-labor but similar issues applied. Several years ago we examined HSP70 expression in placentae from normal and preeclampsia with our without IUGR [23]. Others have preformed immunofluorescence on paraffin sections. HSP 70 expression was reported to be increased in preeclampsia [24]. The presence of a uterine artery notch in a mixed group of normal pregnant, preeclampsia and preeclampsia plus IUGR was associated with increased eNOS and HSP 70 in basal plate samples taken from patients who underwent caesarean section. Placental villous tissue was not studied [25].Some studies have examined HSP 70 expression in early pregnancy. HSP 70 temporarily increases during 8? weeks of gestation when blood flow to the placenta is initiated leading to an oxidative stress insult [26]. HSP 70 immunostaining also increased in early pregnancy miscarriage [27]. Janiaux et al [28] examined HSP 70 and nitrotyrosine expression in placentae obtained from surgically terminated pregnancies between 8?3 weeks of gestation. They sampled the inner and outer third. Immunoreactivity for HSP 70 and nitrotyrosine residues was greater in samples from peripheral than from central regions of normal placentas and from missed miscarriages compared to controls. They proposed that oxidative damage to the trophoblast, induced by premature onset of the maternal placental circulation is a key factor in early pregnancy loss. HSP 70 was reported to be reduced in purified cytotrophoblast 1655472 cells from preeclampsia cases compared to controls however labor and site of sampling was not studied. The shock of enzyme digestion and cell purification are also confounding factors [29]. Since intracellular HSP 70 binds to the progesterone receptor and functions as a co-repressor of this receptor [30] this may in part explain our results providing a mechanism linking HSP 70 to labor. HSF-1 is the stress responsive transcriptional activator responsible for the inducible transcription of genes encoding HSPs [31]. Padmini et al [32] reported increased HSP 70 and HSF-1 in placentae from preeclampsia cases compare with uncomplicated pregnancies. Malyshev et al (1995) [33] showed that oxidative stress increases NFkB which in turn activates nitric oxide synthase, nitric oxide release and subsequently HSP 70 induction in several organs. Blocking nitric oxide synthase activity inhibited HSP 70 induction. We have previously shown that villous eNOS [34], peroxynitrite production [35] and lipid peroxidation [23] are increased in preeclampsia. HSPs can be detected in the circulation. The few reported studies of HSP 70 serum concentrations in preeclampsia and labor are conflicting [30,36]. In summary spatial changes in HSP 70 expression occur during labor and preeclampsia. The physiological and pathological significance of this remains to b.

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