@article{SchieferdeckerPestelPuescheletal.1999,
  author    = {Schieferdecker, Henrike L. and Pestel, Sabine and P{\"u}schel, Gerhard Paul and G{\"o}tze, Otto},
  title     = {Increase by anaphylatoxin C5a of glucose output in perfused rat liver via prostanoids derived from nonparenchymal cells : direct action of prostaglandins and indirect action of thromboxane A(2) on hepatocytes},
  year      = {1999},
  abstract  = {In the perfused rat liver the anaphylatoxin C5a enhanced glucose output, reduced flow, and elevated prostanoid overflow. Because hepatocytes (HCs) do not express C5a receptors, the metabolic C5a actions must be indirect, mediated by e.g. prostanoids from Kupffer cells (KCs) and hepatic stellate cells (HSCs), which possess C5a receptors. Surprisingly, the metabolic C5a effects were not only impaired by the prostanoid synthesis inhibitor, indomethacin, but also by the thromboxane A(2) (TXA(2)) receptor antagonist, daltroban, even though HCs do not express TXA(2) receptors. TXA(2) did not induce prostaglandin (PG) or an unknown factor release from KCs or sinusoidal endothelial cells (SECs), which express TXA(2) receptors, because (1) daltroban did neither influence the C5a-induced release of prostanoids from cultured KCs nor the C5a-dependent activation of glycogen phosphorylase in KC/HC cocultures and because (2) the TXA(2) analog, U46619, failed to stimulate prostanoid release from cultured KCs or SECs or to activate glycogen phosphorylase in KC/HC or SEC/HC cocultures. In the perfused liver, Ca(2+)-deprivation inhibited not only flow reduction but also glucose output elicited by C5a to similar extents as daltroban. Similarly, in the absence of extracellular Ca(2+), flow reduction and glucose output induced by U46619 were almost completely prevented, whereas glucose output induced by the directly acting PGF(2alpha) was only slightly lowered. Thus, in the perfused rat liver PGs released after C5a- stimulation from KCs and HSCs directly activated glycogen phosphorylase in HCs, and TXA(2) enhanced glucose output indirectly mainly by causing hypoxia as a result of flow reduction.},
  language  = {en}
}
@article{FennekohlSchieferdeckerJungermannetal.1999,
  author    = {Fennekohl, Alexandra and Schieferdecker, Henrike L. and Jungermann, Kurt and P{\"u}schel, Gerhard Paul},
  title     = {Differential expression of prostanoid receptors in hepatocytes, Kupffer cells, sinusoidal endothelial cells and stellate cells of rat liver},
  issn      = {0168-8278},
  year      = {1999},
  abstract  = {BACKGROUND/AIMS: Prostanoids produced by nonparenchymal cells modulate the function of parenchymal and nonparenchymal liver cells during homeostasis and inflammation via eight classes of prostanoid receptors coupled to different G-proteins. Prostanoid receptor expression in parenchymal and nonparenchymal cells was studied in order to get a better insight into the complex prostanoid-mediated intrahepatic signaling network. METHODS: RNA was isolated from freshly purified parenchymal and nonparenchymal rat liver cells and the mRNA level of all eight prostanoid receptor classes was determined by newly developed semiquantitative reverse transcription-polymerase chain reaction protocols. RESULTS: The mRNAs for the prostanoid receptors were differentially expressed. Hepatocytes were the only cell type which contained the mRNA of the Gq-linked prostaglandin F2alpha receptor; they were devoid of any mRNA for the Gs-linked prostanoid receptors. Kupffer cells possessed the largest amount of mRNA for the Gs-linked prostaglandin E2 receptor subtype 2. Endothelial cells expressed high levels of mRNA for the Gq-linked thromboxane receptor and medium levels of mRNA for the Gs-linked prostacyclin receptor, while stellate cells had the highest levels of mRNA for the prostacyclin receptor. The mRNAs for the Gq-linked prostaglandin E2 receptor subtype 1 and the Gi-linked prostaglandin E2 receptor subtype 3 were expressed in hepatocytes and all nonparenchymal cell types at similar high levels, whereas the mRNA of the Gs-linked prostaglandin D2 receptor was expressed in all nonparenchymal cells at very low levels. CONCLUSIONS: In hepatocytes the prostaglandin F2alpha receptor can mediate an increase in glucose output via an increase of intracellular InsP3 while cAMP-dependent glucose output can be inhibited via the subtype 3 prostaglandin E2 receptor. The subtype 2 prostaglandin E2 receptor can restrain the inflammatory response of Kupffer cells via an increase in intracellular cAMP The thromboxane receptor and the prostacyclin receptor in sinusoidal endothelial and the prostacyclin receptor in stellate cells may be involved in the regulation of sinusoidal blood flow and filtration.},
  language  = {en}
}