Naked caspase 3 small interfering RNA is effective in cold preservation but not in autotransplantation of porcine kidneys

2013 ◽  
Vol 181 (2) ◽  
pp. 342-354 ◽  
Author(s):  
Cheng Yang ◽  
Yichen Jia ◽  
Tian Zhao ◽  
Yinjia Xue ◽  
Zitong Zhao ◽  
...  
Keyword(s):  
Small Interfering Rna ◽  
Caspase 3 ◽  
Cold Preservation ◽  
Interfering Rna

scholarly journals Gene therapy with caspase-3 small interfering RNA-nanoparticles is neuroprotective after optic nerve damage

2021 ◽  
Vol 16 (12) ◽  
pp. 2534
Author(s):  
BernhardA Sabel ◽  
Mohamed Tawfik ◽  
Xiwei Zhang ◽  
Lisa Grigartzik ◽  
Peter Heiduschka ◽  
...  
Keyword(s):  
Gene Therapy ◽  
Optic Nerve ◽  
Small Interfering Rna ◽  
Caspase 3 ◽  
Nerve Damage ◽  
Optic Nerve Damage ◽  
Interfering Rna

scholarly journals Ketamine Activates Cell Cycle Signaling and Apoptosis in the Neonatal Rat Brain

2010 ◽  
Vol 112 (5) ◽  
pp. 1155-1163 ◽  
Author(s):  
Sulpicio G. Soriano ◽  
Qian Liu ◽  
Jing Li ◽  
Jia-Ren Liu ◽  
Xiao Hui Han ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Death ◽  
Cyclin D1 ◽  
Small Interfering Rna ◽  
Caspase 3 ◽  
Primary Neurons ◽  
Cyclin Dependent Kinase ◽  
Cell Cycle Signaling ◽  
Interfering Rna

Background Prolonged exposure to ketamine results in accelerated neurodegeneration and neurocognitive deficits in the neonatal rats. Experimental models of neurodegeneration have implicated reentry of postmitotic neurons into the cell cycle, leading to cell death. The authors hypothesize that the ketamine-induced neuroapoptosis is partially due to aberrant cycle cell reentry. To explore this hypothesis, the authors characterized the effect of ketamine on the cell cycle signaling pathway in the developing rodent brain in vivo and in vitro. Methods Postnatal day 7 rat pups and primary neurons were used for the experiments. Each rat pup received five intraperitoneal doses of either saline or ketamine (5, 10, and 20 mg/kg/dose) at 90-min intervals over 6 h. Primary neurons were exposed to varying concentrations of ketamine to determine the dose and duration effects. The expression of cell cycle proteins (cyclin D1, cyclin-dependent kinase 4, and E2F1), Bcl2-interacting mediator of cell death (Bim), and activated caspase-3 was determined. The effect of cyclin D1 knockdown by small interfering RNA was also examined in primary neurons incubated in ketamine. Results Ketamine mediated a dose- and time-dependent increase in expression of cell cycle proteins and activated caspase-3. Cyclin D1, cyclin-dependent kinase 4, E2F1, Bim, and cleaved caspase-3 expression increased at 12 h and peaked at 24 h in vitro. Knockdown of cyclin D1 by small interfering RNA attenuated Bim and cleaved caspase-3 expression. Conclusion These findings support a model in which ketamine induces aberrant cell cycle reentry, leading to apoptotic cell death in the developing rat brain.

scholarly journals Zearalenone Induces Endothelial Cell Apoptosis through Activation of a Cytosolic Ca2+/ERK1/2/p53/Caspase 3 Signaling Pathway

Toxins ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 187
Author(s):  
Hyeon-Ju Lee ◽  
Se-Young Oh ◽  
Inho Jo
Keyword(s):  
Signaling Pathway ◽  
Small Interfering Rna ◽  
Caspase 3 ◽  
Cytosolic Calcium ◽  
Receptor Activation ◽  
Oxygen Species ◽  
Endothelial Cell Apoptosis ◽  
Induced Apoptosis ◽  
Interfering Rna ◽  
Specific Inhibitors

Zearalenone (ZEN) is a mycotoxin that has been reported to damage various types of cells/tissues, yet its effects on endothelial cells (ECs) have never been investigated. Therefore, this study investigates the potential effects of ZEN using bovine aortic ECs (BAECs). In this study, we found that ZEN induced apoptosis of BAECs through increased cleavage of caspase 3 and poly ADP-ribose polymerase (PARP). ZEN also increased phosphorylation of ERK1/2 and p53, and treatment with the ERK1/2 or p53 inhibitor reversed ZEN-induced EC apoptosis. Transfection of BAECs with small interfering RNA against ERK1/2 or p53 revealed ERK1/2 as an upstream target of p53 in ZEN-stimulated apoptosis. ZEN increased the production of reactive oxygen species (ROS), yet treatment with the antioxidant did not prevent EC apoptosis. Similarly, blocking of estrogen receptors by specific inhibitors also did not prevent ZEN-induced apoptosis. Finally, chelation of cytosolic calcium (Ca2+) using BAPTA-AM or inhibition of endoplasmic reticulum (ER) Ca2+ channel using 2-APB reversed ZEN-induced EC apoptosis, but not by inhibiting ER stress using 4-PBA. Together, our findings demonstrate that ZEN induces EC apoptosis through an ERK1/2/p53/caspase 3 signaling pathway activated by Ca2+ release from the ER, and this pathway is independent of ROS production and estrogen receptor activation.

scholarly journals HSPB1 Promotes Doxorubicin-induced Cardiomyocyte Pyroptosis by Inhibiting AATF

2021 ◽  
Author(s):  
Yao Tang ◽  
Yaxiu Liu ◽  
Shuang Fu ◽  
Xinbin Zheng ◽  
Mingrui Li ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Heat Shock ◽  
Adverse Effects ◽  
Small Interfering Rna ◽  
Therapeutic Strategy ◽  
Caspase 3 ◽  
Shock Proteins ◽  
Interfering Rna ◽  
Novel Therapeutic

Abstract Background: Doxorubicin (DOX) has been widely used for the treatment of different kinds of cancers. However, the adverse effects, especially cardiotoxicity, which limit the long-term use of DOX. Although some signaling pathways have been investigated to be participated in DOX-induced cardiotoxicity, however, the mechanisms underlying DOX-induced cardiotoxicity need to be further investigated. Recent study suggested that heat shock proteins (HSPs) play a role in cell apoptosis and pyroptosis. However, we do not know yet whether heat shock protein beta-1 (HSPB1), a member of HSPs family, is involved in DOX-induced cardiomyocyte pyroptosis. This study aimed to evaluate the effects of HSPB1 and apoptosis antagonizing transcription factor (AATF) in DOX-induced pyroptosis in cardiomycytes.Results: We found that DOX remarkably enhanced the expression of HSPB1 but reduces AATF expression in cardiomyocytes. We also found that either inhibition of HSPB1 by small interfering RNA (siRNA) or overexpression of AATF by transfection of AATF plasmid significantly attenuated DOX-induced cardiomyocyte pyroptosis. Moreover, HSPB1 interacts with AATF. Furthermore, inhibition of HSPB1 and AATF restores the DOX-induced cardiomyocyte pyroptosis. Conclusion: Our findings reveal a novel pathway that cardiomyocyte pyroptosis is regulated through HSPB1-AATF-caspase-3-GSDME pathway following DOX treatment, suggesting that HSPB1-AATF-dependent pyroptosis may provide a novel therapeutic strategy to reduce cardiotoxicity induced by DOX.

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