RGD Reference Report - [The effect of transmembrane- and secreted-tumor necrosis factor-alpha on shock liver] - Rat Genome Database

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[The effect of transmembrane- and secreted-tumor necrosis factor-alpha on shock liver]

Authors: Yin, B  Li, Z  Yu, S  Jiang, X  Feng, W  Xu, Y 
Citation: Yin B, etal., Zhonghua Bing Li Xue Za Zhi. 2002 Dec;31(6):534-7.
RGD ID: 1598936
Pubmed: PMID:12622907   (View Abstract at PubMed)

OBJECTIVE: To observe the dynamic expression of transmembrane (TM)-tumor necrosis factor (TNF)-alpha and secreted (S)-TNF-alpha in the development of endotoxic shock and explore the actions and mechanism of TM-TNF-alpha in liver of the rat with endotoxic shock. METHODS: Endotoxic shock in rats was induced by intravenous injection of dead gram negative bacteria E. Coli; the kinetics of TM-TNF-alpha on peritoneal macrophages and S-TNF-alpha in serum of these rats were determined. Pretreatment with TNF alpha converting enzyme antisense oligonucleotide (5 mg/kg) 30 minutes before rats were administrated dead bacteria inhibited enzymatic cleavage of TM-TNF-alpha into S-TNF-alpha. Six hours after bacteria injection, TM-TNF-alpha and S-TNF-alpha were also detected respectively. The pathological injury in the livers of rats with endotoxin shock was examined, and artery pressure was constantly measured. RESULTS: The kinetics of TM-TNF-alpha expression in the development of endotoxic shock was different from that of S-TNF-alpha expression in serum. The expression of TM-TNF-alpha began to increase on the surface of peritoneal macrophages and liver within 30 min, after bacteria challenge and peaking within a period of 4.5 hours followed by a gradual decrease to a relatively high level which was maintained for at least 24 hours. The TACE antisense oligonucleotide pretreated rats showed remarkable increase in TM-TNF-alpha expression by peritoneal macrophages and liver (P < 0.001), and their arterial blood pressure were maintained within normal levels and there were no detectable pathological changes in their livers. CONCLUSIONS: These findings suggested that TM-TNF-alpha may be a potent endogenous regulator involved in anti-inflammatory responses to maintain normal arterial pressure and protect liver tissue from pathological injury in during endotoxin shock. This study confirmed the important role of TNF-alpha in endotoxic shock which is not only of important theoretical significance, but also of practical interest in providing experimental basis for clinical treatment of endotoxin shock.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
toxic shock syndrome  ISOTnf (Rattus norvegicus)1598936; 1598936protein:increased expression:peritoneal macrophage and cell surface (rat)RGD 
toxic shock syndrome  IEP 1598936protein:increased expression:peritoneal macrophage and cell surface (rat)RGD 

Gene Ontology Annotations    Click to see Annotation Detail View

Cellular Component
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
external side of plasma membrane  IDA 1598936 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Tnf  (tumor necrosis factor)

Genes (Mus musculus)
Tnf  (tumor necrosis factor)

Genes (Homo sapiens)
TNF  (tumor necrosis factor)


Additional Information