Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0022116 (
ischemia
)
91,303
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Increased inflammatory responses and enhanced reactive oxygen species contribute to hepatic
ischemia
/reperfusion (I/R) injury, however the modulatory mechanisms haven't been completely unveiled. Here, we report that genetic deficiency of
MAPK-activated protein kinase 2
(
MK2
) protected against hepatic I/R injury and decreased hepatic neutrophil accumulation in
MK2
-/-
mice. Depletion of neutrophil attenuated hepatic I/R injury in wide type mice. In response to C5a stimulation,
MK2
-/-
neutrophils generated less superoxide in which both NADPH oxidase activation and p47
phox
phosphorylation were decreased. Furthermore, Ser329 of p47
phox
was identified for enhancement of superoxide production. The Ser329 phosphorylation was reduced in
MK2
-/-
neutrophils. To determine whether
MK2
modulates hepatic I/R injury via activating neutrophils, we generated myeloid-specific
MK2
deletion mice (
MK2
Lyz2-KO
) and liver I/R injury was reduced in
MK2
Lyz2-KO
mice. Our results indicate that
MK2
augments hepatic I/R injury and induces ROS production with increased p47
phox
phosphorylation and
MK2
is a potential drug target for treating hepatic I/R injury.
...
PMID:A Role for MK2 in Enhancing Neutrophil-Derived ROS Production and Aggravating Liver Ischemia/Reperfusion Injury. 3048 68
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