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At least 865 records · Page 48Linked to original sources
PubMed1987

Inositol phospholipid turnover and protein kinase C translocation are stimulated by poly(I).poly(C) in human amnion cells (UAC).

Polyinosinic-polycytidylic acid, a potent inducer of inducer of interferon (IFN) production and activator of some IFN-induced enzymes, inhibits [3H]uridine incorporation into the RNA of vesicular stomatitis virus even in the absence of IFN synthesis, transiently triggers the breakdown of inositol phospholipids and activates the translocation of protein kinase C. Since IFNs also have similar activities these results suggest that IFN induction and IFN function are realised through common biochemical pathways.

Amnion↗
PubMed1987

IL2-like material is present in human placenta and amnion.

Human term placenta was shown to react with different polyclonal and monoclonal anti-interleukin 2 (IL2) antibodies by using indirect immunofluorescence on frozen sections. Labelling was localized on syncytiotrophoblast membrane, amniotic epithelium and cytotrophoblast of the reactivity [corrected]. The reproducibility of the observations with different basal plate. These features were observed with two different rabbit anti-IL2 polyclonal antibodies, a sheep IL2 antiserum and 15.2, an anti-IL2 monoclonal antibody. However, DMS-1, a second anti-IL2 monoclonal antibody, did not react. Pre-incubation of anti-IL2 sera with IL2 resulted in the disappearance of syncytiotrophoblast reactivity. The reproducibility of the observations with different reagents strongly suggests that the recognized molecule shares several epitopes with IL2. However, it has not been possible to demonstrate the presence of a conventional IL2 receptor by using two monoclonal antibodies directed to the 55 kDa chain of IL2 receptor.

Amnion↗
PubMed2004

Stimulation of early gene induction and cell proliferation by lysophosphatidic acid in human amnion-derived WISH cells: role of phospholipase D-mediated pathway.

Human-amniotic WISH cells express the lysophosphatidic acid (LPA) receptor, LPA(1), LPA(2) but not LPA(3). When WISH cells were stimulated with LPA, phospholipase D (PLD) activation was dramatically induced via a cytosolic calcium increase and protein kinase C activation. We also found that LPA stimulated two kinds of mitogen-activated protein kinase (MAPK), extracellular signal-regulated kinase (ERK) and p38 kinase via PLD-dependent signaling pathways in WISH cells. In terms of the LPA-mediated functional modulation of WISH cells, we observed that LPA stimulates the induction of two early genes (c-Jun and c-Fos) and cellular proliferation in WISH cells. We examined the signaling pathways involved in LPA-mediated cellular responses. LPA-induced early gene induction was completely blocked by normal butanol (n-butanol) but not by t-butanol, suggesting that PLD activity is essentially required for the process. PD98059 (2'-amino-3'-methoxyflavone) but not SB203580 (4-(4-fluorophenyl)-2-(4-methylsulfinylphenyl)-5-(4-pyridyl)1H-imidazole) also significantly blocked LPA-induced early gene induction, suggesting a crucial role for ERK. Pertussis toxin (PTX) did not affect on the LPA-induced early gene induction and ERK activation, ruling out the role of Gi/o protein(s) in the process. The cellular proliferation of WISH cells was also dramatically inhibited by n-butanol or PD98059. This study demonstrates the physiological role of LPA on the modulation of early gene induction and on WISH cell proliferation, and the crucial role played by PLD in the process.

Amnion↗
PubMed2004

Thickening of the amnion basement membrane and its relationship to placental inflammatory lesions and fetal and maternal disorders.

OBJECTIVE: The aim of this study is the morphological and morphometric analysis of the basement membrane amniotic epithelium of the chorionic plate to establish possible correlation between the basement membrane amniotic epithelium thickening and maternal and fetal disorders. STUDY DESIGN: Ninety-one placentas of infants delivered in Medical Hospital School were studied with hematoxylin-eosin (H&E) and Periodic Acid Schiff (PAS) methods, morphometric and ultrastructural analysis. RESULTS: Of the 91 placentas analyzed, 17 (18.6%) were normal with regard to placental morphology, fetal and maternal history. Basement membrane amniotic epithelium thickening was significantly greater in the cases associated with chorioamnionitis (P=0.013), villitis (P=0.040), maternal hypertension syndromes during pregnancy (P=0.027) and stillborn (P=0.040) babies. The electron microscopic examination of the basement membrane amniotic epithelium identified a structural alteration and edema of the dense lamina. CONCLUSION: Thickening of the basement membrane amniotic epithelium was associated with morphologic placental abnormalities and/or fetal or maternal disorders. Thickening of the basement membrane amniotic epithelium was identified away from the site of placental inflammation, possibly being a consequence of cytokines, supporting more than a local effect. This could be a new insight into the pathogenesis of fetal and maternal complications associated with inflammatory placental lesions.

Adult↗