Soluble Fas gene therapy protects against Fas-mediated apoptosis of hepatocytes but not the lethal effects of Fas-induced TNF-α production by ... View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2002-05-24

AUTHORS

Y Matsuki, L Li, H-C Hsu, P A Yang, R Zheng, C K Edwards, I H Chaudry, H-G Zhang, J D Mountz

ABSTRACT

The elevation of soluble Fas (sFas) in the sera of patients with liver disease suggests a role for sFas in the disease process; whether it is protective or not is controversial. To determine the effects of sFas on Fas-induced liver apoptosis, we manipulated mice to produce sFas by transfecting them in vivo with different amounts of an adenovirus that produces mouse sFas driven by the CMV promoter (AdsFas). Fas-mediated apoptosis was induced by administration of anti-mouse Fas (Jo2; 10 μg/mouse) one week later. The administration of AdsFas (103, 107, or 109 pfu/mouse), which was associated with only minimal side-effects, resulted in a significant reduction in the liver transaminase levels and mortality of the mice on challenge with Jo2, as compared to control mice treated with AdLacZ. However, the protective effect of AdsFas was not complete. The possibility that Jo2-induction of TNF-α in the Kupffer cells of the liver contributes to the pathology was therefore tested. Although administration of soluble TNF receptor (sTNFRI) alone did not protect the mice from the lethal effects of Jo2, administration of sTNFRI (200 μg/mouse) after infection with AdsFas (109 pfu/mouse) resulted in 100% survival of the mice on challenge with Jo2. To confirm that the production of TNF-α by Kupffer cells produce the lethal effects of Jo2 that remained after treatment with AdsFas, these cells were selectively ablated by treatment of the mice with gadolinium chloride prior to challenge with Jo2. This treatment greatly reduced early mortality and hepatocellular damage as well as TNF-α production 6 h after injection of Jo2. These results indicate that: (1) AdsFas prevents Jo2-induced apoptosis of hepatocytes; (2) In addition to mediating Fas-mediated apoptosis of hepatocytes, Jo2 can separately induce TNF-α production by Kupffer cells resulting in early mortality, and (3) Optimal protection from Jo2-induced mortality can be achieved by protection of liver cells by pretreatment with both AdsFas and sTNFRI. More... »

PAGES

626-635

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/sj.cdd.4401016

DOI

http://dx.doi.org/10.1038/sj.cdd.4401016

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1030089876

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/12032671


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76 injection of Jo2
77 lethal effects
78 levels
79 liver
80 liver apoptosis
81 liver cells
82 liver disease
83 liver transaminase levels
84 mice
85 mortality
86 mouse sFas
87 one week
88 optimal protection
89 pathology
90 patients
91 possibility
92 pretreatment
93 process
94 production
95 production 6
96 production of TNF
97 promoter
98 protection
99 protective effect
100 protects
101 receptors
102 reduction
103 results
104 role
105 sTNFRI
106 sera of patients
107 serum
108 significant reduction
109 soluble Fas
110 soluble TNF receptors
111 survival
112 therapy protects
113 transaminase levels
114 treatment
115 vivo
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