Nicotine induces H9C2 cell apoptosis via Akt protein degradation
Autor: | Huaning Xie, Rui An, Xiong Guo, Shan Wang, Huishou Zhao, Xiaomeng Zhang, Kun Lian, Feng Yan, Chong Huang, Jinglong Zhang, Ling Tao |
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Rok vydání: | 2017 |
Předmět: |
0301 basic medicine
Nicotine Proteasome Endopeptidase Complex Cancer Research Small interfering RNA Cell Survival Down-Regulation AKT1 Apoptosis Biology Biochemistry Cell Line 03 medical and health sciences Genetics medicine Animals E2F1 Myocytes Cardiac RNA Messenger Viability assay RNA Small Interfering Molecular Biology Protein kinase B Ubiquitin Cell cycle Rats Up-Regulation Cell biology 030104 developmental biology Oncology Proteolysis Molecular Medicine Proto-Oncogene Proteins c-akt Signal Transduction medicine.drug |
Zdroj: | Molecular Medicine Reports. 16:6269-6275 |
ISSN: | 1791-3004 1791-2997 |
DOI: | 10.3892/mmr.2017.7331 |
Popis: | Smoking is highly associated with cardiovascular diseases. However, the effect of nicotine, a key ingredient in smoking products, on cardiomyocyte apoptosis remains controversial. The present study aims to clarify the role of nicotine on cardiomyocyte cell apoptosis and to investigate the underlying mechanism. In the present study, H9C2 cells were exposed to nicotine at various concentrations (0, 10 and 100 µM) for 48 h. Cell Counting Kit‑8 and TUNEL assays were performed to assess cell viability and apoptosis, respectively, and reverse transcription‑quantitative polymerase chain reaction and western blot analysis were used to investigate the mRNA and protein expression. PYR‑41, a ubiquitin E1 inhibitor, was employed to investigate whether the ubiquitin‑proteasome system was involved in the downregulation of Akt. An Akt1 overexpression plasmid was used to demonstrate the role of Akt in H9C2 cells apoptosis. Tetratricopeptide repeat domain 3 (TTC3) small interfering RNA (siRNA) was used to investigate the effect of TTC3 on Akt protein degradation. The results demonstrated that nicotine induced apoptosis in H9C2 cells compared with control cells (P |
Databáze: | OpenAIRE |
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