Lentiviral-mediated p38 MAPK RNAi attenuates aldosterone-induced myocyte apoptosis

Zhou, Yan; Wei, Jie; Chen, Jing; Tang, Qi‐Zhu

doi:10.3892/mmr.2013.1539

Cited by 4 publications

(4 citation statements)

References 25 publications

(33 reference statements)

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“…Studies have revealed that aldosterone directly induces myocyte apoptosis through the p38 MAPK signaling pathway, which in turn exerts a protective effect on aldosterone-induced myocyte apoptosis. 44 Activation of the p38 MAPK signaling pathway can induce myocardial cell apoptosis, which is consistent with the findings of the present study. Therefore, the p38 MAPK signaling pathway is potentially the pathway associated with promotion of cardiomyocyte apoptosis in a rabbit susceptibility model of hyperthyroidism-induced AF following sympathetic activation.…”

Section: Discussionsupporting

confidence: 93%

Sympathetic Activation Promotes Cardiomyocyte Apoptosis in a Rabbit Susceptibility Model of Hyperthyroidism-Induced Atrial Fibrillation via the p38 MAPK Signaling Pathway

Zheng

Zhao²,

Yang³

et al. 2023

Crit Rev Eukaryot Gene Expr

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Excess thyroid hormone secretion can cause endocrine metabolic disorders, which can lead to cardiovascular diseases, including heart enlargement, atrial fibrillation (AF), and heart failure. The present study investigated the molecular mechanisms of hyperthyroidism-induced AF. A rabbit susceptibility model of hyperthyroidism-induced AF was constructed, and metoprolol treatment was administered. Norepinephrine levels were determined using enzyme-linked immunosorbent assay; quantitative reverse transcription polymerase chain reaction and immunohistochemistry were used to detect the expression of markers for sympathetic remodeling (growth associated protein 43 and tyrosine hydroxylase in atrial myocardial tissues and stellate ganglia). Primary rabbit cardiomyocytes were cultured and identified by immunofluorescence staining, and terminal deoxynucleotidyl transferase dUTP nick end labeling staining was used to measure cardiomyocyte apoptosis; western blot was used to detect the expression of apoptosis-related proteins, including Bax, Bcl-2, and cleaved caspase-3, as well as to measure the phosphorylation states of p38 mitogen-activated protein kinase (MAPK) pathway proteins. Metoprolol inhibited sympathetic activation and cardiomyocyte apoptosis in the rabbit model by inhibiting the p38 MAPK signaling pathway. Immunofluorescence staining results revealed that the rabbit cardiomyocytes were isolated successfully. Inhibition of p38 MAPK signaling alleviated norepinephrine-induced apoptosis in cardiomyocytes. Sympathetic activation promotes apoptosis in cardiomyocytes with hyperthyroidism-induced AF via the p38 MAPK signaling pathway. The results of the present study provide a novel theoretical basis for the potential clinical treatment of patients with hyperthyroidism and AF.

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Section: Discussionsupporting

confidence: 93%

Sympathetic Activation Promotes Cardiomyocyte Apoptosis in a Rabbit Susceptibility Model of Hyperthyroidism-Induced Atrial Fibrillation via the p38 MAPK Signaling Pathway

Zheng

Zhao²,

Yang³

et al. 2023

Crit Rev Eukaryot Gene Expr

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“…Knockdown of Prx V expression in HT22 cells enhanced glutamate-induced decreases in cell viability and increased cellular apoptosis, which may be associated with increases in the cellular ROS levels. The MAPK signaling pathway is widely involved in cell proliferation, migration, apoptosis and differentiation, and has been reported to be closely associated with cellular ROS levels (35)(36)(37). However, to the best of our knowledge, no previous evidence has demonstrated an association between Prx V and MAPK in neuronal cell apoptosis.…”

Section: Discussionmentioning

confidence: 89%

Knockdown of peroxiredoxin V increases glutamate‑induced apoptosis in HT22 hippocampal neuron cells

Shen

Liu

Li³

et al. 2018

Mol Med Report

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High concentrations of glutamate may mediate neuronal cell apoptosis by increasing intracellular reactive oxygen species (ROS) levels. Peroxiredoxin V (Prx V), a member of the Prx family, serves crucial roles in protecting cells from oxidative stress. The present study investigated the regulatory effect of Prx V on glutamate‑induced effects on viability and apoptosis in HT22 cells. Western blotting was used for protein expression analysis and Annexin V/PI staining and flow cytometry for determination of apoptosis. The results demonstrated that glutamate may ROS‑dependently increase HT22 cell apoptosis and upregulate Prx V protein levels. Furthermore, knockdown of Prx V protein expression with a lentivirus significantly enhanced HT22 cell apoptosis mediated by glutamate, which was reversed by inhibition of ROS with N‑acetyl‑L‑cysteine. Inhibiting the extracellular signal‑regulated kinase (ERK) signaling pathway with PD98059, a specific inhibitor for ERK phosphorylation, markedly decreased glutamate‑induced HT22 cell apoptosis in Prx V knockdown cells, indicating the potential involvement of ERK signaling in glutamate‑induced HT22 cell apoptosis. In addition, an increase in nuclear apoptosis‑inducing factor was observed in Prx V knockdown HT22 cells following glutamate treatment, compared with mock cells, whereas no differences in B‑cell lymphoma‑2 and cleaved‑caspase‑3 protein expression levels were observed between mock and Prx V knockdown cells. The results of the present study indicated that Prx V may have potential as a therapeutic molecular target for glutamate‑induced neuronal cell death and provide novel insight into the role of Prx V in oxidative‑stress induced neuronal cell death.

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“…The role of p38 in cancer depends on the cell type and cancer stage. Certain studies have reported that p38 increases cell proliferation, whereas in others, the activation of the MAPK p38 pathway is described as tumor suppressive (29)(30)(31)(32)(33)(34). In the present study, the p38 pathway was observed to exhibit a tumor suppressive role in HCC.…”

Section: Discussionmentioning

confidence: 99%

Mitogen-activated protein kinase kinase 3 induces cell cycle arrest via p38 activation mediated Bmi-1 downregulation in hepatocellular carcinoma

Wang

Chen

Feng

et al. 2015

Molecular Medicine Reports

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The underlying molecular pathogenesis of hepatocellular carcinoma (HCC) remains poorly understood. Mitogen-activated protein kinase kinase 3 (MKK3), has been reported as a novel tumor suppressor in breast cancer. However, its potential suppressive role in HCC has not been evaluated. In the current study, the biologic functions of MKK3 in HCC were investigated and a previously unreported cell cycle regulation mechanism was observed. MKK3 overexpression suppressed HepG2 and PLC‑PRF‑5 cell proliferation and induced cell cycle arrest in the two cell lines. In addition, MKK3 overexpression upregulated the cyclin-dependent kinase inhibitors, p16 INK4A and p15 INK4B in HCC cells. Their negative regulator, Bim‑1, was downregulated following MKK3 overexpression. Moreover, MKK3 activated p38 in HCC cells and SB203580, a p38 inhibitor, reversed the tumor suppressive effect of MKK3. In conclusion, the results identify MKK3 as a tumor suppressor and highlighted the significance of p38 pathway aberration in HCC.

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Lentiviral-mediated p38 MAPK RNAi attenuates aldosterone-induced myocyte apoptosis

Cited by 4 publications

References 25 publications

Sympathetic Activation Promotes Cardiomyocyte Apoptosis in a Rabbit Susceptibility Model of Hyperthyroidism-Induced Atrial Fibrillation via the p38 MAPK Signaling Pathway

Sympathetic Activation Promotes Cardiomyocyte Apoptosis in a Rabbit Susceptibility Model of Hyperthyroidism-Induced Atrial Fibrillation via the p38 MAPK Signaling Pathway

Knockdown of peroxiredoxin V increases glutamate‑induced apoptosis in HT22 hippocampal neuron cells

Mitogen-activated protein kinase kinase 3 induces cell cycle arrest via p38 activation mediated Bmi-1 downregulation in hepatocellular carcinoma

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