Inhibition of Na+/H+ exchanger isoform 1 attenuates mitochondrial cytochrome C release in cortical neurons following in vitro ischemia

2006 ◽  
pp. 244-248 ◽  
Author(s):  
J. Luo ◽  
H. Chen ◽  
D. B. Kintner ◽  
G. E. Shull ◽  
D. Sun
Keyword(s):  
Cytochrome C ◽  
Cortical Neurons ◽  
Mitochondrial Cytochrome ◽  
Cytochrome C Release ◽  
In Vitro Ischemia ◽  
Mitochondrial Cytochrome C

Inhibitory action of Wnt target gene osteopontin on mitochondrial cytochrome c release determines renal ischemic resistance

2010 ◽  
Vol 299 (1) ◽  
pp. F234-F242 ◽  
Author(s):  
Jose Luis Viñas ◽  
Anna Sola ◽  
Michaela Jung ◽  
Chrysoula Mastora ◽  
Eugenia Vinuesa ◽  
...  
Keyword(s):  
Cytochrome C ◽  
Wnt Pathway ◽  
Brown Norway ◽  
Mitochondrial Cytochrome ◽  
Cytochrome C Release ◽  
Norway Rats ◽  
Mitochondrial Cytochrome C

Certain determinants of ischemic resistance in the Brown Norway rat strain have been proposed, but no studies to date have focused on the role of the Wnt pathway in the ischemic resistance mechanism. We performed a comparative genomic study in Brown Norway vs. Sprague-Dawley rats. Selective manipulations of the Wnt pathway in vivo and in vitro allowed us to study whether the action of the Wnt pathway on apoptosis through the regulation of osteopontin was critical to the maintenance of inherent ischemic resistance mechanisms. The results revealed a major gene upregulation of the Wnt family in Brown Norway rats after renal ischemia-reperfusion. Manipulation of the Wnt signaling cascade by selective antibodies increased mitochondrial cytochrome c release and caspase 3 activity. The antiapoptotic role of Wnt was mediated by osteopontin, a direct Wnt target gene. Osteopontin was reduced by Wnt antibody administration in vivo, and osteopontin gene silencing in vitro significantly increased mitochondrial cytochrome c release. The overexpression of Wnt pathway genes detected in Brown Norway rats is critical in the maintenance of their inherent ischemic resistance. Activation of the Wnt signaling cascade reduces mitochondrial cytochrome c release and caspase 3 activity through the action of osteopontin.

Platycodon grandiflorum Induces Apoptosis in SKOV3 Human Ovarian Cancer Cells Through Mitochondrial-Dependent Pathway

2010 ◽  
Vol 38 (02) ◽  
pp. 373-386 ◽  
Author(s):  
Qin Hu ◽  
Ruile Pan ◽  
Liwei Wang ◽  
Bo Peng ◽  
Jingtian Tang ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cytochrome C ◽  
Cancer Cells ◽  
Caspase 3 ◽  
Ovarian Cancer Cells ◽  
Mitochondrial Cytochrome ◽  
Cytochrome C Release ◽  
Apoptotic Pathway ◽  
Platycodon Grandiflorum ◽  
Mitochondrial Cytochrome C

Platycodon grandiflorum (Jacq.) A. DC., a Chinese food and medicine, has been used as expectorant traditionally. The present study aimed to investigate the effect of Platycodon grandiflorum extract (PGE) on SKOV3 ovarian cancer cells. 3-(4,5- dimethylthiazol-2-yl)-2,5- diphenyltetrazolium bromide (MTT) assay was used to monitor cell numbers, Annexin-V/propidium iodide (PI) staining, RT-PCR and Western blot were used to examine cell apoptosis, caspases activation. Bcl-2 and Bax expressions and mitochondrial cytochrome c release. Our result showed that PGE-induced apoptosis was associated with activation of caspase-3, -8 and -9, down-regulation of Bcl-2, up-regulation of Bax and release of mitochondrial cytochrome c to cytosol. The data indicate that PGE may have anti-tumor effect mainly via caspase-3 and caspase-9 dependent apoptotic pathway.

Regional expression of Bcl-2 mRNA and mitochondrial cytochrome c release after experimental brain injury in the rat

2001 ◽  
Vol 903 (1-2) ◽  
pp. 45-52 ◽  
Author(s):  
Gao-Xiang Dong ◽  
Dev K Singh ◽  
Peter Dendle ◽  
Renuka M Prasad
Keyword(s):  
Brain Injury ◽  
Cytochrome C ◽  
Mitochondrial Cytochrome ◽  
Cytochrome C Release ◽  
Mitochondrial Cytochrome C

Cytochrome c release into cytosol with subsequent caspase activation during warm ischemia in rat liver

2001 ◽  
Vol 281 (4) ◽  
pp. G1115-G1123 ◽  
Author(s):  
Junpei Soeda ◽  
Shinichi Miyagawa ◽  
Kenji Sano ◽  
Junya Masumoto ◽  
Shun'Ichiro Taniguchi ◽  
...  
Keyword(s):  
Cytochrome C ◽  
Dna Fragmentation ◽  
Warm Ischemia ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Dependent Manner ◽  
Mitochondrial Cytochrome ◽  
Caspase Activation ◽  
Cytochrome C Release ◽  
Apoptotic Pathway ◽  
Mitochondrial Cytochrome C

Apoptosis plays an important role in liver ischemia and reperfusion (I/R) injury. However, the molecular basis of apoptosis in I/R injury is poorly understood. The aims of this study were to ascertain when and how apoptotic signal transduction occurs in I/R injury. The apoptotic pathway in rats undergoing 90 min of warm ischemia with reperfusion was compared with that of rats undergoing prolonged ischemia alone. During ischemia, mitochondrial cytochrome c was released into the cytosol in a time-dependent manner in hepatocytes and sinusoidal endothelial cells, and caspase-3 and an inhibitor of caspase-activated DNase were cleaved. However, apoptotic manifestation and DNA fragmentation were not observed. After reperfusion, nuclear condensation, cells positive for terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling, and DNA fragmentation were observed and caspase-8 and Bid cleavage occurred. In contrast, prolonged ischemia alone induced necrosis rather than apoptosis. In summary, our results show that release of mitochondrial cytochrome c and caspase activation proceed during ischemia, although apoptosis is manifested after reperfusion.

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