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  • Cy5 carboxylic acid (non-sulfonated) Where does this transfe


    Where does this transfer process occur? The maternal side of the placenta is textured and spongy looking. The surface has 20–30 distinctive compartments named cotyledons, inside of which are the chorionic villi that form the principal functional structural unit of the placenta. These villi are complex tree-like structures that contain fetal blood. The intervillous space is filled by maternal blood. Each cotyledon contains at least one villous tree. The trophoblast separates the maternal from the fetal blood and forms the large outer surface of the villi that constitutes the area for exchange; here is where the transport processes take place. The trophoblast separates the maternal and fetal blood and thus may be viewed as an epithelium, since it effectively segregates two fluid compartments. However, the trophoblast differs from the majority of epithelial Cy5 carboxylic acid (non-sulfonated) in that it has no lateral membranes, being a syncytium. As depicted in Fig. 1, a section of the tip of a single branch of the villous tree shows the syncytiotrophoblast as a big, multinucleate polarized cell. Transcellular transport across the syncytiotrophoblast requires movement across both its maternal-facing apical (microvillous) plasma membrane and the fetal-facing basal plasma membrane. All solutes transported across the placenta, including chloride ions, must cross through the placental syncytiotrophoblast, thus it constitutes the main placental barrier to exchange between mother and fetus during pregnancy.
    First evidence for chloride channels in the placenta Chloride transport in the placenta has been studied mainly in isolated syncytiotrophoblast membrane vesicles from term placentae. Initially, the experiments were focused on the characteristics of Cl− fluxes in microvillous membrane vesicles derived from normal term placentae [9], [10], [11], [12], [13], [14], [15], [16]. The data from this preparation showed that about 50% of chloride transport occurred by Cl−/HCO3− exchange [11], [9]. However, the remaining flux was dependent on membrane potential and suggested the possibility that it may take place through a conductive pathway [17], [10], [16]. Subsequent detailed studies of chloride fluxes and ionic dependence of the membrane potential have confirmed the presence of chloride-conductive pathways in the microvillous membrane [18], [19], [14], [15]. Byrne [13] suggested that uptake of chloride across the microvillous membrane of human placenta may occur by at least, three different pathways: an electroneutral anion exchanger, a diphenylamine-2-carboxylic acid (DPC)-sensitive conductance and a 4,4′diisothiocyanostilbene-2, 2′-disulphonic acid (DIDS)-sensitive conductance. Both DIDS and DPC are blockers of certain types of chloride channels. These experiments corroborated previous results from Dechecchi [11] and Illsley [16], where the DIDS-sensitive and the DIDS-insensitive components of chloride transport were voltage-dependent, and the latter component was inhibited by DPC. These properties, sensitivity to both membrane potential and specific chloride channels blockers, definitively indicated the presence of conductive pathways for chloride transfer across the microvillous membrane of hSTB. Consequently, Stulc in his review on placental ion transport [20] incorporated three main mechanisms of chloride uptake across the apical membrane, where two of them were chloride-conductive pathways. During this period of flux studies, there was also considerable interest in the regulation of the chloride conductances in apical membrane vesicles from human placenta. It has been suggested that apical membrane chloride conductances are inhibited by protein kinase A-dependent phosphorylation [14] and by unsaturated fatty acids such as arachidonic and linoleic acid [19], [18], [21]. However, in order to identify which types of channels are specifically regulated in placental membranes and to determine their biophysical properties, it was necessary to develop new experiments involving electrophysiological and molecular biology methods that could contribute to identifying the channels that underlie these conductances.