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CaMKII δ Deletion Protects Against Apoptosis In Myocardial Ischemia/Reperfusion Injury In Vivo
Author(s) -
Ling Haiyun,
Zhang Tong,
Brown Joan Heller
Publication year - 2008
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.22.1_supplement.730.16
Subject(s) - dna laddering , apoptosis , in vivo , ischemia , reperfusion injury , blot , knockout mouse , chemistry , pharmacology , microbiology and biotechnology , medicine , biology , programmed cell death , dna fragmentation , biochemistry , gene , receptor
Background: The δ subunit of Ca 2 + /Calmodulin‐dependent protein kinase II (CaMKII) predominates in the heart. There is controversy regarding the role of CaMKII in myocardial ischemia/reperfusion, based largely on in vitro experiments using a pharmacological CaMKII inhibitor (KN‐93). The best evidence for in vivo function of CaMKII would come from the use of mice in which the gene is deleted. A mouse with CaMKII δ deletion has been recently developed in our lab. Methods and Results: CaMKII δ knockout mice and littermate controls were subjected to 1 h myocardial ischemia followed by 6 h reperfusion. Infarct size was measured by Evans blue/TTC staining. Apoptosis was assayed by DNA laddering. The expression of apoptosis related proteins (caspase‐3 and Bax) was also examed by Western blotting. Compared to WT controls, mice in which CaMKII δ was deleted showed a significant reduction in infarct size and DNA laddering, accompanied by attenuated Bax and caspase‐3 in the ischemic myocardium. Conclusion: CaMKII δ deletion protects against apoptosis in myocardial ischemia/reperfusion injury in vivo . This work was supported by HL80101.