scholarly journals A murine platelet-activating factor receptor gene: cloning, chromosomal localization and up-regulation of expression by lipopolysaccharide in peritoneal resident macrophages

1996 ◽  
Vol 314 (2) ◽  
pp. 671-678 ◽  
Author(s):  
Satoshi ISHII ◽  
Yoichi MATSUDA ◽  
Motonao NAKAMURA ◽  
Iwao WAGA ◽  
Kazuhiko KUME ◽  
...  
Keyword(s):  
Lipid A ◽  
Receptor Gene ◽  
Platelet Activating Factor ◽  
Peritoneal Macrophages ◽  
Regulation Of Expression ◽  
Gene Encoding ◽  
Platelet Activating Factor Receptor ◽  
Factor Α ◽  
Necrosis Factor

A murine gene encoding a platelet-activating factor receptor (PAFR) was cloned. The gene was mapped to a region of the D2.2 band of chromosome 4 both by fluorescence in situ hybridization and by molecular linkage analysis. Northern blot analysis showed a high expression of the PAFR message in peritoneal macrophages. When C3H/HeN macrophages were treated with bacterial lipopolysaccharide (LPS) or synthetic lipid A, the PAFR gene expression was induced. Bacterial LPS, but not lipid A, induced the level of PAFR mRNA in LPS-unresponsive C3H/HeJ macrophages. These induction patterns were parallel to those of tumour necrosis factor-α mRNA. Thus the PAFR in macrophages is important in LPS-induced pathologies.

scholarly journals Effects of esculentoside A on turnour necrosis factor production by mice peritoneal macrophages

1992 ◽  
Vol 1 (6) ◽  
pp. 375-377 ◽  
Author(s):  
Fang Jun ◽  
Zheng Qin Yue ◽  
Wang Hong Bin ◽  
Ju Dian Wen ◽  
Yi Yang Hua
Keyword(s):  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Inflammatory Mediator ◽  
Platelet Activating Factor ◽  
Peritoneal Macrophages ◽  
Dependent Manner ◽  
Anti Inflammatory ◽  
Dose Dependent ◽  
Necrosis Factor ◽  
Inflammatory Effect

Esculentoside A (EsA) is a saponin isolated from the roots of Phytolacca esculenta. Previous experiments showed that it had strong anti-inflammatory effects. Tumour necrosis factor (TNF) is an important inflammatory mediator. In order to study the mechanism of the anti-inflammatory effect of EsA, it was determined whether TNF production from macrophages was altered by EsA under lipopolysaccharide (LPS) stimulated conditions. EsA was found to decrease both extracellular and cell associated TNF production in a dose dependent manner at concentrations higher than 1 μmol/l EsA. Previous studies have showed that EsA reduced the releasing of platelet activating factor (PAF) from rat macrophages. The reducing effects of EsA on the release of TNF and PAF may explain its anti-inflammatory effect.

Tumor necrosis factor-α mRNA and protein in endometrial tumors: Analysis by in situ hybridization and immunocytochemistry

1994 ◽  
Vol 25 (12) ◽  
pp. 1324-1331 ◽  
Author(s):  
F.U. Garcia ◽  
H.-L. Chen ◽  
Y. Yang ◽  
J.L. Pace ◽  
X.-L. Hu ◽  
...  
Keyword(s):  
In Situ Hybridization ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Factor Α ◽  
Necrosis Factor

Activated Kupffer cells cause a hypermetabolic state after gentle in situ manipulation of liver in rats

2001 ◽  
Vol 280 (6) ◽  
pp. G1076-G1082 ◽  
Author(s):  
Peter Schemmer ◽  
Nobuyuki Enomoto ◽  
Blair U. Bradford ◽  
Hartwig Bunzendahl ◽  
James A. Raleigh ◽  
...  
Keyword(s):  
Liver Transplantation ◽  
Kupffer Cells ◽  
Cell Function ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Hypermetabolic State ◽  
Hypoxia Marker ◽  
Factor Α ◽  
Necrosis Factor

Harvesting trauma to the graft dramatically decreases survival after liver transplantation. Since activated Kupffer cells play a role in primary nonfunction, the purpose of this study was to test the hypothesis that organ manipulation activates Kupffer cells. To mimic what occurs with donor hepatectomy, livers from Sprague-Dawley rats underwent dissection with or without gentle organ manipulation in a standardized manner in situ. Perfused livers exhibited normal values for O2 uptake (105 ± 5 μmol · g−1 · h−1) measured polarigraphically; however, 2 h after organ manipulation, values increased significantly to 160 ± 8 μmol · g−1 · h−1 and binding of pimonidazole, a hypoxia marker, increased about threefold ( P < 0.05). Moreover, Kupffer cells from manipulated livers produced three- to fourfold more tumor necrosis factor-α and PGE2, whereas intracellular calcium concentration increased twofold after lipopolysaccharide compared with unmanipulated controls ( P < 0.05). Gadolinium chloride and glycine prevented both activation of Kupffer cells and effects of organ manipulation. Furthermore, indomethacin given 1 h before manipulation prevented the hypermetabolic state, hypoxia, depletion of glycogen, and release of PGE2 from Kupffer cells. These data indicate that gentle organ manipulation during surgery activates Kupffer cells, leading to metabolic changes dependent on PGE2 from Kupffer cells, which most likely impairs liver function. Thus modulation of Kupffer cell function before organ harvest could be beneficial in human liver transplantation and surgery.

scholarly journals Cytogenetic and syntenic assignment of the bovine <i>platelet-activating factor receptor (PTAFR)</i> to cattle chromosome 2 (Brief report)

2009 ◽  
Vol 52 (4) ◽  
pp. 448-450
Author(s):  
T. Goldammer ◽  
P. Schmidt ◽  
R. Weikard
Keyword(s):  
Bos Taurus ◽  
Hybrid Cell ◽  
Platelet Activating Factor ◽  
Chromosome 2 ◽  
Cattle Chromosome ◽  
Reproduction Process ◽  
Somatic Hybrid Cell ◽  
Platelet Activating Factor Receptor ◽  
Pathologic Processes

Abstract. The platelet-activating factor receptor (PTAFR) encoding gene, also known as PAFR or PAFr, belongs to the rhodopsin gene family. The receptor binds the platelet-activating factor (PAF) that has been implicated as a mediator in diverse pathologic processes. In cattle, PTAFR is associated to the reproduction process and is described as a receptor that is involved in inflammatory-like processes of the uterus associated with increased vascular permeability (TIEMANN et al. 2005). The gene sequence was recently annotated on Bos taurus (BTA) chromosome 2 at 129.4 megabases in NCBI Bos taurus build Btau_4.0. The presented data confirm this annotation by independent physical mapping methods and anchor the corresponding DNA segment to the chromosome. PTAFR was assigned by fluorescence in situ hybridization (FISH) and somatic hybrid cell (SHC) mapping.

scholarly journals Tumor necrosis factor/cachectin stimulates peritoneal macrophages, polymorphonuclear neutrophils, and vascular endothelial cells to synthesize and release platelet-activating factor.

1987 ◽  
Vol 166 (5) ◽  
pp. 1390-1404 ◽  
Author(s):  
G Camussi ◽  
F Bussolino ◽  
G Salvidio ◽  
C Baglioni
Keyword(s):  
Endothelial Cells ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Vascular Endothelial Cells ◽  
Platelet Activating Factor ◽  
Peritoneal Macrophages ◽  
Dermal Fibroblasts ◽  
Polymorphonuclear Neutrophils ◽  
Vascular Endothelial ◽  
Necrosis Factor

Murine tumor necrosis factor (mTNF) stimulates production of platelet-activating factor (PAF) by cultured rat peritoneal macrophages in amounts comparable to those formed during treatment with the calcium ionophore A23187 or phagocytosis of zymosan. The cell-associated PAF that was released into the medium was identical to synthetic PAF, as determined with physicochemical, chromatographic, and enzymatic assays. Furthermore, de novo synthesis of PAF by macrophages was demonstrated by the incorporation of radioactive precursors such as [3H]acetyl-coenzyme A or [3H]2-lyso-PAF. Macrophages incubated with mTNF for 4 h synthesized PAF only during the first h of treatment. At this time, the amount of cell-associated PAF was approximately equal to that released into the medium. The cell-associated PAF decreased afterwards, whereas that in the medium did not correspondingly increase, suggesting that some PAF was being degraded. The response of rat macrophages to different doses of mTNF and human TNF (hTNF) was examined. Maximal synthesis of PAF was obtained with 10 ng/ml of mTNF and 50 ng/ml of hTNF. This finding may be explained by a lower affinity of hTNF for TNF receptors of rat cells. The hTNF stimulated production of PAF by human vascular endothelial cells cultured from the umbilical cord vein. The time course of PAF synthesis was slower than that observed with macrophages, with maximal production between 4 and 6 h of treatment. Optimal synthesis of PAF was obtained with 10 ng/ml of hTNF. Only 20-30% of the PAF synthesized by endothelial cells was released into the medium, even after several hours of incubation. Synthesis of PAF in response to TNF was also detected in rat polymorphonuclear neutrophils, but not in human tumor cells and dermal fibroblasts. Therefore, production of PAF is a specialized response that is transient in macrophages continuously treated with TNF, and that appears to be controlled by unidentified regulatory mechanisms.

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