GTP-binding protein mediated phospholipase A(2) activation in rat liver during the progression of sepsis

Citation
Lj. Tong et al., GTP-binding protein mediated phospholipase A(2) activation in rat liver during the progression of sepsis, MOL C BIOCH, 189(1-2), 1998, pp. 55-61
Citations number
35
Categorie Soggetti
Cell & Developmental Biology
Journal title
MOLECULAR AND CELLULAR BIOCHEMISTRY
ISSN journal
03008177 → ACNP
Volume
189
Issue
1-2
Year of publication
1998
Pages
55 - 61
Database
ISI
SICI code
0300-8177(199812)189:1-2<55:GPMPAA>2.0.ZU;2-7
Abstract
Effects of GTP-binding proteins on the activation of secretory phospholipas eA, (sPLA(2)) and cytosolic phospholipaseA, (cPLA(2)) in rat liver during t wo different phases of sepsis were studied. Sepsis was induced by cecal lig ation and puncture (CLP). Experiments were divided into three groups: contr ol, early sepsis, and late sepsis. Early and late sepsis refers to those an imals sacrificed at 9 and 18 h, respectively, after CLP. The results show t hat in the absence of G-protein modulator, hepatic sPLA(2) and cPLA(2) acti vities were activated by 40.8-46 and 91.6-105.8%, respectively, during earl y and late phases of sepsis. GTP gamma S and fluoroaluminate (AlF4-) stimul ated sPLA(2) and cPLA(2) activities within each experimental group, i.e., c ontrol, early sepsis, and late sepsis. The GTP gamma S and AlF4--stimulated sPLA(2) and cPLA(2) activities remained significantly elevated during earl y phase (22.3-65.6% increase) and late phase (32.5-109.1% increase) of seps is. Further analyses demonstrate that cholera toxin significantly stimulate d sPLA(2) and cPLA(2) activities within each experimental group, and that t he cholera toxin stimulated sPLA(2) and cPLA(2) activities remained signifi cantly higher during early phase (23.5-37% increase) and late phase (56.7-7 0% increase) of sepsis. In contrast, pertussis toxin significantly inhibite d sPLA(2) and cPLA(2) activities within each experimental group, and that t he pertussis toxin-inhibited sPLA(2) and cPLA(2) activities remained signif icantly higher in early septic (57-68.5% increase) and late septic (34.6-45 .5% increase) experiments. These data demonstrate that cholera toxin-sensit ive Gas and pertussis toxin-sensitive G alpha i were both involved in the a ctivation of sPLA(2) and cPLA(2) activities in rat liver during the progres sion of sepsis.