Protective effect of adenovirus-mediated heat shock protein 70 gene transfection against hypoxia/reoxygenation injury of cultured neonatal rat myocardiocytes

2010 ◽  
Vol 29 (12) ◽  
pp. 1344-1348
Author(s):  
Wei YU ◽  
Yu YAN ◽  
Yu-dong ZHANG ◽  
Qing NI
2000 ◽  
Vol 32 (12) ◽  
pp. 2229-2237 ◽  
Author(s):  
Ken-ichiro Kawana ◽  
Yuki Miyamoto ◽  
Kouichi Tanonaka ◽  
Yoko Han-no ◽  
Hiroyuki Yoshida ◽  
...  

2016 ◽  
Vol 11 (7) ◽  
pp. 1134 ◽  
Author(s):  
Yan Qu ◽  
Yuan Liu ◽  
Xue-chun Wang ◽  
Dan Hu ◽  
Shu-ran Huang ◽  
...  

2013 ◽  
Vol 28 (3) ◽  
pp. 269-277 ◽  
Author(s):  
Yilong Dong ◽  
Yanmei Wang ◽  
Haijing Yu ◽  
Yanyong Liu ◽  
Nan Yang ◽  
...  

2013 ◽  
Vol 699 (1-3) ◽  
pp. 67-73 ◽  
Author(s):  
Kwok-Keung Lam ◽  
Pao-Yun Cheng ◽  
Yen-Mei Lee ◽  
Yu-Pei Liu ◽  
Cheng Ding ◽  
...  

2008 ◽  
Vol 294 (1) ◽  
pp. H249-H256 ◽  
Author(s):  
Courtney L. Williamson ◽  
Erinne R. Dabkowski ◽  
Wolfgang H. Dillmann ◽  
John M. Hollander

The majority of mitochondrial proteins are encoded by nuclear genes and synthesized in the cytosol as preproteins containing a mitochondria import sequence. Preproteins traverse the outer mitochondrial membrane in an unfolded state and then translocate through the inner membrane into the matrix via import machinery that includes mitochondrial heat shock protein 70 (mtHSP70). Neonatal rat cardiac myocytes (NCM) infected with an adenoviral vector expressing mtHSP70 or an empty control (Adv−) for 48 h were submitted to 8 h of simulated ischemia (hypoxia) followed by 16 h of reperfusion (reoxygenation). Infection with mtHSP70 virus yielded an increase in mtHSP70 protein in NCM mitochondria compared with Adv−( P < 0.05). Cell viability after simulated ischemia/reperfusion (I/R) was decreased in both Adv−and mtHSP70 groups, relative to control ( P < 0.05), but mtHSP70-infected NCM had enhanced viability after I/R relative to Adv-infected NCM ( P < 0.05). Simulated I/R caused an increase in reactive oxygen species generation and lipid peroxidation in Adv-infected NCM ( P < 0.05, for both) that was not observed in mtHSP70-infected NCM. Mitochondrial complex III and IV activities were greater in mtHSP70-infected NCM after simulated I/R compared with Adv−( P < 0.05 for both). After simulated I/R, ATP content increased in mtHSP70-infected NCM, compared with Adv−( P < 0.05). Apoptotic markers were decreased in mtHSP70-infected NCM compared with Adv−after simulated I/R ( P < 0.05). These results indicate that overexpression of mtHSP70 protects the mitochondria against damage from simulated I/R that may be due to a decrease in reactive oxygen species leading to preservation of mitochondrial complex function activities and ATP formation.


Circulation ◽  
2001 ◽  
Vol 104 (suppl 1) ◽  
pp. I-303-I-307 ◽  
Author(s):  
Jay Jayakumar ◽  
Ken Suzuki ◽  
Ivan A. Sammut ◽  
Ryszard T. Smolenski ◽  
Mak Khan ◽  
...  

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