NDLI: Divergent results induced by different types of septic shock in transglutaminase 2 knockout mice

Content Provider	Springer Nature Link
Author	Yoo, Hyun Ahn, Eu Ree Kim, Se Jin Lee, Seon Hyeong Oh, Seung Hyun Kim, Soo Youl
Copyright Year	2012
Abstract	Acute sepsis can be induced by cytokines such as TNF-α and biological products such as LPS. All of these agents cause systemic inflammation, which is characterized by hemodynamic shock and liver toxicity. However, the outcomes of different septic shock models were totally opposite in transglutaminase 2 knockout (TGase 2−/−) mice. The aim of our study was to clarify the role of TGase 2 in liver injury. Therefore, we explored the role of TGase 2 in liver damage using two different stress models: LPS-induced endotoxic shock and TNF-α/actinomycin D (ActD)-induced sepsis. TNF-α-dependent septic shock resulted in increased liver damage in TGase 2−/− mice compared with wild-type (WT) mice, and was accompanied by increased levels of caspase 3 and cathepsin D (CTSD) in the damaged liver. Conversely, LPS-induced septic shock resulted in ablation of inflammatory endotoxic shock in TGase 2−/− mice and decreased liver injury. We found that TGase 2 protected liver tissue from TNF-α-dependent septic shock by reducing the expression of caspase 3 and CTSD. However, TGase 2 differently participated in increased the hemodynamic shock in LPS-induced septic shock through macrophage activation rather than protecting direct liver damage. Therefore, these findings demonstrate that septic shock caused by different agents may induce different results in TGase 2−/− mice depending on the primary target organs affected.
Starting Page	189
Ending Page	197
Page Count	9
File Format	PDF
ISSN	09394451
Journal	Amino Acids
Volume Number	44
Issue Number	1
e-ISSN	14382199
Language	English
Publisher	Springer Vienna
Publisher Date	2012-10-10
Publisher Place	Vienna
Access Restriction	Subscribed
Subject Keyword	Transglutaminase Acute liver failure TNF-α Cathepsin D Caspase 3 Biochemistry Analytical Chemistry Biochemical Engineering Life Sciences Proteomics Neurobiology
Content Type	Text
Resource Type	Article
Subject	Organic Chemistry Biochemistry Clinical Biochemistry

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