scholarly journals Inhibition of cell death in the intervertebral disc by caspase 3 small interfering RNA

2011 ◽  
Vol 63 (6) ◽  
pp. 1477-1478 ◽  
Author(s):  
A. Hari Reddi
Keyword(s):  
Cell Death ◽  
Intervertebral Disc ◽  
Small Interfering Rna ◽  
Caspase 3 ◽  
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.

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 The MAPK Kinase Kinase-1 Is Essential for Stress-Induced Pancreatic Islet Cell Death

Endocrinology ◽  
2008 ◽  
Vol 149 (6) ◽  
pp. 3046-3053 ◽  
Author(s):  
Dariush Mokhtari ◽  
Jason W. Myers ◽  
Nils Welsh
Keyword(s):  
Cell Death ◽  
Small Interfering Rna ◽  
Islet Cells ◽  
Β Cell ◽  
Pancreatic Islet Cell ◽  
Mapk Kinase ◽  
Transient Overexpression ◽  
Novel Therapeutic Strategies ◽  
Interfering Rna

The aim of the present investigation was to characterize the role of the MAPK kinase kinase-1 (MEKK-1) in stress-induced cell death of insulin producing cells. We observed that transient overexpression of the wild type MEKK-1 protein in the insulin-producing cell lines RIN-5AH and βTC-6 increased c-Jun N-terminal kinase (JNK) phosphorylation and augmented cell death induced by diethylenetriamine/nitroso-1-propylhydrazino)-1-propanamine (DETA/NO), streptozotocin (STZ), and hydrogen peroxide (H2O2). Furthermore, DETA/NO or STZ induced a rapid threonine phosphorylation of MEKK-1. Silencing of MEKK-1 gene expression in βTC-6 and human dispersed islet cells, using in vitro-generated diced small interfering RNA, resulted in protection from DETA/NO, STZ, H2O2, and tunicamycin induced cell death. Moreover, in DETA/NO-treated cells diced small interfering RNA-mediated down-regulation of MEKK-1 resulted in decreased activation of JNK but not p38 and ERK. Inhibition of JNK by treatment with SP600125 partially protected against DETA/NO- or STZ-induced cell death. In summary, our results support an essential role for MEKK-1 in JNK activation and stress-induced β-cell death. Increased understanding of the signaling pathways that augment or diminish β-cell MEKK-1 activity may aid in the generation of novel therapeutic strategies in the treatment of type 1 diabetes.

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 ClC5 Decreases the Sensitivity of Multiple Myeloma Cells to Bortezomib via Promoting Prosurvival Autophagy

2018 ◽  
Vol 26 (3) ◽  
pp. 421-429 ◽  
Author(s):  
Huimin Zhang ◽  
Yuhui Pang ◽  
Chuanbao Ma ◽  
Jianying Li ◽  
Huaquan Wang ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Cell Death ◽  
Small Interfering Rna ◽  
Critical Role ◽  
Treatment Strategies ◽  
Myeloma Cell ◽  
Beclin 1 ◽  
Myeloma Cells ◽  
Multiple Myeloma Cell ◽  
Interfering Rna

Resistance to bortezomib (BZ) is the major problem that largely limits its clinical application in multiple myeloma treatment. In the current study, we investigated whether ClC5, a member of the chloride channel family, is involved in this process. The MTT assay showed that BZ treatment decreased cell viability in three multiple myeloma cell lines (ARH77, U266, and SKO-007), with IC50 values of 2.83, 4.37, and 1.91 nM, respectively. Moreover, BZ increased the conversion of LC3B-I to LC3B-II and expressions of beclin-1 and ATG5, concomitantly with a decreased p62 expression. Pharmacological inhibition of autophagy with 3-MA facilitated cell death in response to BZ treatment. Additionally, BZ increased ClC5 protein expression in ARH77, U266, and SKO-007 cells. Knockdown of ClC5 with small interfering RNA sensitized cells to BZ treatment, and upregulation of ClC5 induced chemoresistance to BZ. Furthermore, ClC5 downregulation promoted BZ-induced LC3B-I to LC3B-II conversion and beclin-1 expression, whereas overexpression of ClC5 showed the opposite results in ARH77 cells. Finally, BZ induced dephosphorylation of AKT and mTOR, which was significantly attenuated by ClC5 inhibition. However, ClC5 upregulation further enhanced AKT and mTOR dephosphorylation induced by BZ. Our study demonstrates that ClC5 induces chemoresistance of multiple myeloma cells to BZ via increasing prosurvival autophagy by inhibiting the AKT‐mTOR pathway. These data suggest that ClC5 may play a critical role in future multiple myeloma treatment strategies.

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