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Downregulation of cardiac lineage protein‐1 confers cardioprotection through the upregulation of redox effectors
Author(s) -
Gurusamy Narasimman,
Lekli Istvan,
Ahsan Md. Kaimul,
Ray Diptarka,
Mukherjee Subhendu,
Mascareno Eduardo,
Siddiqui M.A.Q.,
Das Dipak K.
Publication year - 2010
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2009.11.054
Subject(s) - cardioprotection , downregulation and upregulation , thioredoxin , glutaredoxin , microbiology and biotechnology , effector , chemistry , reperfusion injury , ischemia , biology , biochemistry , oxidative stress , medicine , gene
CLP‐1, the mouse homologue of human Hexim1 protein, exerts inhibitory control on transcriptional elongation factor‐b of RNA transcript elongation. Previously, we have demonstrated that downregulation of cardiac lineage protein‐1 (CLP‐1) in CLP‐1 +/− heterozygous mice affords cardioprotection against ischemia–reperfusion injury. Our current study results show that the improvement in cardiac function in CLP‐1 +/− mice after ischemia–reperfusion injury is achieved through the potentiation of redox signaling and their molecular targets including redox effector factor‐1, nuclear factor erythroid 2‐related factor, and NADPH oxidase 4 and the active usage of thioredoxin‐1, thioredoxin‐2, glutaredoxin‐1 and glutaredoxin‐2. Our results suggest that drugs designed to down regulate CLP‐1 could confer cardioprotection through the potentiation of redox cycling.