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Adenosine A1 receptors induce translocation of PKC ε to the caveolar membrane of cardiac myocytes
Author(s) -
Yang Zhaogang,
Garg Vivek,
Hu Keli
Publication year - 2009
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.23.1_supplement.lb39
Subject(s) - caveolae , adenosine , myocyte , adenosine receptor , protein kinase c , caveolin 3 , microbiology and biotechnology , medicine , adenosine a1 receptor , receptor , endocrinology , caveolin , chemistry , biology , signal transduction , agonist
Caveolae are specialized microdomains of the plasma membrane. They play an important role in the cardioprotective effect of ischemic preconditioning. Both adenosine receptors and PKC ε , which have been shown to reside in the caveolae of cardiac myocytes, are associated with ischemic preconditioning. However, the potential link between adenosine receptors and PKC ε has not been elucidated. The present study was designed to test the hypothesis that adenosine A1 receptors induce the translocation of PKC ε to the plasma membrane within caveolae. Immunoblot analysis from the homogenate of freshly isolated cardiac myocytes revealed that the intensity of 100 kD band corresponding to PKC ε increased significantly in the membrane fractions in cells pretreated with adenosine (100 μM) when compared with non‐stimulated cells. The effect of adenosine on PKC ε translocation was blocked by a specific A1 antagonist 8‐cyclopentyl‐1,3‐dipropylxanthine (DPCPX, 1 μM). Western blot in caveolin‐enriched fractions prepared from isolated cardiac myocytes showed that immunoreactivity for PKC ε increased significantly from cells treated with adenosine but not with adenosine plus DPCPX. Furthermore, PKC ε was detected in the anti‐caveolin‐3 immunoprecipitates from caveolar fractions. In conclusion, we demonstrate that activation of adenosine A1 receptors promotes the translocation of PKC ε to the caveolin‐enriched plasma membrane of cardiac myocytes.