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The involvement of guanylyl cyclase‐G in intestinal ischemia and reperfusion‐induced jejunal apoptosis in mice
Author(s) -
Lo HuiChen,
Yang RueyBing,
Huang YuChan,
Lai ChunHong
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.102.7
Subject(s) - apoptosis , jejunum , cytochrome c , endocrinology , medicine , ischemia , chemistry , cytosol , signal transduction , intestinal ischemia , reperfusion injury , biology , biochemistry , enzyme
Our previous study indicated that guanylyl cyclase (GC)‐G gene plays a certain role in maintaining jejunal morphology and regulating systemic and local inflammatory responses. In this study, we further investigated the molecular mechanism of GC‐G gene in modulating intestinal apoptosis. Sham operation and 45 min intestinal ischemia with 3h, 6h, 12h, or 24h reperfusion were performed in both male WT and KO mice. Our results showed that KO mice had significantly increased protein expressions of active caspase‐3 (17kDa), cytochrome c, and Bax in the jejunum compared to WT mice before intestinal I/R injury. After suffering from intestinal I/R, active caspase‐3, Bax, and Bcl‐2 were significantly increased at 3h and reversed at 12h in WT mice, whereas those were significantly decreased at 12h in KO mice. There was no significant difference in cytosol IκBα between WT and KO mice before and after intestinal I/R; however, nuclear phosphorylated NFκB was significantly decreased at 24h in KO mice compared to WT mice. In addition, intestinal I/R‐induced increases in phosphorylated JNK1 and Erk1 were occurred at 3h in WT mice and 6h in KO mice. Taken together, our results demonstrated that KO mice have attenuated changes in intestinal morphology and apoptosis signaling pathways when suffered from intestinal I/R. These results suggest that mGC‐G plays important roles in maintaining jejunal morphology and regulating apoptosis.