Role of Caveolin-3 and Glucose Transporter-4 in Isoflurane-induced Delayed Cardiac Protection
| Autor: | Brian P. Head, Yoshitaka Kawaraguchi, Ingrid R. Niesman, Piyush M. Patel, Hemal H. Patel, Yousuke T. Horikawa, David M. Roth, Blake Chin-Lee, Michael W. Kidd, Yasuo M. Tsutsumi |
|---|---|
| Rok vydání: | 2010 |
| Předmět: |
Male
medicine.medical_specialty Cardiotonic Agents Time Factors Caveolin 3 Myocardial Infarction Myocardial Reperfusion Injury Article Mice Random Allocation In vivo Caveolae Internal medicine Caveolin medicine Animals Myocytes Cardiac Mice Knockout Glucose Transporter Type 4 Isoflurane business.industry Glucose transporter Mice Inbred C57BL Anesthesiology and Pain Medicine Endocrinology Anesthesia Ischemic Preconditioning Myocardial Anesthetic Knockout mouse business medicine.drug |
| Zdroj: | Anesthesiology. 112:1136-1145 |
| ISSN: | 0003-3022 |
| Popis: | Background Caveolae are small, flask-like invaginations of the plasma membrane. Caveolins are structural proteins found in caveolae that have scaffolding properties to allow organization of signaling. The authors tested the hypothesis that delayed cardiac protection induced by volatile anesthetics is caveolae or caveolin dependent. Methods An in vivo mouse model of ischemia-reperfusion injury with delayed anesthetic preconditioning (APC) was tested in wild-type, caveolin-1 knockout, and caveolin-3 knockout mice. Mice were exposed to 30 min of oxygen or isoflurane and allowed to recover for 24 h. After 24 h recovery, mice underwent 30-min coronary artery occlusion followed by 2 h of reperfusion at which time infarct size was determined. Biochemical assays were also performed in excised hearts. Results Infarct size as a percent of the area at risk was reduced by isoflurane in wild-type (24.0 +/- 8.8% vs. 45.1 +/- 10.1%) and caveolin-1 knockout mice (27.2 +/- 12.5%). Caveolin-3 knockout mice did not show delayed APC (41.5 +/- 5.0%). Microscopically distinct caveolae were observed in wild-type and caveolin-1 knockout mice but not in caveolin-3 knockout mice. Delayed APC increased the amount of caveolin-3 protein but not caveolin-1 protein in discontinuous sucrose-gradient buoyant fractions. In addition, glucose transporter-4 was increased in buoyant fractions, and caveolin-3/glucose transporter-4 colocalization was observed in wild-type and caveolin-1 knockout mice after APC. Conclusions These results show that delayed APC involves translocation of caveolin-3 and glucose transporter-4 to caveolae, resulting in delayed protection in the myocardium. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|