scholarly journals Expression of the skeletal muscle dystrophin–dystroglycan complex and syntrophin-nitric oxide synthase complex is severely affected in the type 2 diabetic Goto–Kakizaki rat

2005 ◽  
Vol 84 (11) ◽  
pp. 867-883 ◽  
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Claire Mulvey ◽  
Erika Harno ◽  
Alan Keenan ◽  
Kay Ohlendieck
2005 ◽  
Vol 90 (2) ◽  
pp. 1100-1105 ◽  
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Sangeeta R. Kashyap ◽  
Linda J. Roman ◽  
Jennifer Lamont ◽  
Bettie Sue S. Masters ◽  
Mandeep Bajaj ◽  
...  

2010 ◽  
Vol 8 (5) ◽  
pp. 459-463 ◽  
Author(s):  
Sangeeta R. Kashyap ◽  
Linda J. Roman ◽  
Lawrence Mandarino ◽  
Ralph DeFronzo ◽  
Mandeep Bajaj

2012 ◽  
Author(s):  
Karla Punkt ◽  
Katharina Kandt ◽  
Andreas Oberbach ◽  
Volker Adams ◽  
Igor Buchwalow ◽  
...  

2013 ◽  
Vol 115 (4) ◽  
pp. 389-393 ◽  
Author(s):  
Karla Punkt ◽  
Katharina Kandt ◽  
Andreas Oberbach ◽  
Volker Adams ◽  
Igor Buchwalow ◽  
...  

2013 ◽  
Vol 231 (3) ◽  
pp. 217-222 ◽  
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Siti Safiah Mokhtar ◽  
Paul M. Vanhoutte ◽  
Susan W.S. Leung ◽  
Mohd Imran Yusof ◽  
Wan Azman Wan Sulaiman ◽  
...  

2018 ◽  
Vol 128 (1) ◽  
pp. 117-129 ◽  
Author(s):  
Zhi-Dong Ge ◽  
Yingchuan Li ◽  
Shigang Qiao ◽  
Xiaowen Bai ◽  
David C. Warltier ◽  
...  

Abstract Background Diabetes impairs the cardioprotective effect of volatile anesthetics, yet the mechanisms are still murky. We examined the regulatory effect of isoflurane on microRNA-21, endothelial nitric-oxide synthase, and mitochondrial respiratory complex I in type 2 diabetic mice. Methods Myocardial ischemia/reperfusion injury was produced in obese type 2 diabetic (db/db) and C57BL/6 control mice ex vivo in the presence or absence of isoflurane administered before ischemia. Cardiac microRNA-21 was quantified by real-time quantitative reverse transcriptional–polymerase chain reaction. The dimers and monomers of endothelial nitric-oxide synthase were measured by Western blot analysis. Mitochondrial nicotinamide adenine dinucleotide fluorescence was determined in Langendorff-perfused hearts. Results Body weight and fasting blood glucose were greater in db/db than C57BL/6 mice. Isoflurane decreased left ventricular end-diastolic pressure from 35 ± 8 mmHg in control to 23 ± 9 mmHg (P = 0.019, n = 8 mice/group, mean ± SD) and elevated ±dP/dt 2 h after post-ischemic reperfusion in C57BL/6 mice. These beneficial effects of isoflurane were lost in db/db mice. Isoflurane elevated microRNA-21 and the ratio of endothelial nitric-oxide synthase dimers/monomers and decreased mitochondrial nicotinamide adenine dinucleotide levels 5 min after ischemia in C57BL/6 but not db/db mice. MicroRNA-21 knockout blocked these favorable effects of isoflurane, whereas endothelial nitric-oxide synthase knockout had no effect on the expression of microRNA-21 but blocked the inhibitory effect of isoflurane preconditioning on nicotinamide adenine dinucleotide. Conclusions Failure of isoflurane cardiac preconditioning in obese type 2 diabetic db/db mice is associated with aberrant regulation of microRNA-21, endothelial nitric-oxide synthase, and mitochondrial respiratory complex I.


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