Shenxiong glucose injection inhibits H2O2-induced H9c2 cell apoptosis by activating the ERK signaling pathway

Abstract Chronic hypoxia is a common inducer of end-stage cardiovascular disease. In cells under hypoxia, the hypoxia-inducible factor-1 (HIF-1) plays a vital role in regulating downstream target genes. However, the mechanism of hypoxia in cardiomyocytes is still unclear. In this study, we aimed to identify novel downstream epigenetic targets of HIF-1α in cardiomyocytes under hypoxia. H9c2 cells were exposed to hypoxia condition, and quantitative real-time PCR analysis was performed to evaluate the expression of miR-20b-5p. The results indicated that the expression of miR-20b-5p was down-regulated in H9c2 cells under low oxygen condition. Meanwhile, HIF-1α overexpression further down-regulated the miR-20b-5p expression in H9c2 cells transfected with HIF-1α plasmids. In addition, Annexin-V-FITC/PI flow cytometry analysis suggested that overexpression of miR-20b-5p attenuated cell apoptosis under hypoxia condition in H9c2 cells. Western blot analysis showed that the hypoxia apparently increased Bax and cleaved-caspase-3, but decreased Bcl-2 expression in H9c2 cells, indicating that hypoxia-induced NF-κB signaling pathway activation is mediated by miR-20b-5p. Hypoxia-induced H9c2 cell apoptosis was reduced after HIF-1α knockdown as shown by the flow cytometry analysis. In conclusion, we identified that miR-20b-5p plays an important role in mediating cardiomyocytes apoptosis under hypoxia, which is mediated by the HIF-1/NF-κB signaling pathway.

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NCAPH promotes cell proliferation and inhibits cell apoptosis of bladder cancer cells through MEK/ERK signaling pathway

Cell Cycle ◽

10.1080/15384101.2021.2021050 ◽

2022 ◽

pp. 1-12

Author(s):

Bo Li ◽

Qian Xiao ◽

Liping Shan ◽

Yongsheng Song

Keyword(s):

Cell Proliferation ◽

Bladder Cancer ◽

Cancer Cells ◽

Signaling Pathway ◽

Cell Apoptosis ◽

Erk Signaling ◽

Bladder Cancer Cells

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Palmitate induces H9c2 cell apoptosis by increasing reactive oxygen species generation and activation of the ERK1/2 signaling pathway

Molecular Medicine Reports ◽

10.3892/mmr.2013.1276 ◽

2013 ◽

Vol 7 (3) ◽

pp. 855-861 ◽

Cited By ~ 17

Author(s):

CHUAN-DONG WEI ◽

YAN LI ◽

HONG-YUN ZHENG ◽

YONG-QING TONG ◽

WEN DAI

Keyword(s):

Reactive Oxygen Species ◽

Signaling Pathway ◽

Cell Apoptosis ◽

Reactive Oxygen Species Generation ◽

Reactive Oxygen ◽

H9c2 Cell ◽

Oxygen Species

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MicroRNA-144 Regulates Cardiomyocyte Proliferation and Apoptosis by Targeting TBX1 through the JAK2/STAT1 Pathway

Cytogenetic and Genome Research ◽

10.1159/000505143 ◽

2019 ◽

Vol 159 (4) ◽

pp. 190-200 ◽

Cited By ~ 1

Author(s):

Mei-Ling Cao ◽

Bin-Lu Zhu ◽

Yuan-Yuan Sun ◽

Guang-Rong Qiu ◽

Wei-Neng Fu ◽

...

Keyword(s):

Cell Proliferation ◽

Signaling Pathway ◽

Cell Apoptosis ◽

Luciferase Reporter Assay ◽

Luciferase Reporter ◽

H9c2 Cell ◽

Reporter Assay ◽

Regulatory Relationship ◽

Tbx1 Gene ◽

Stat1 Signaling

It is currently believed that the TBX1 gene is one of the core genes of congenital heart disease (CHD). However, there are few studies on the abnormal regulation of TBX1 gene expression. The purpose of this work was to investigate the role of miR-144 and TBX1 in cardiac development by studying the regulatory relationship and mechanism of miR-144 on TBX1/JAK2/STAT1 in cardiomyocytes. Cell proliferation was detected by MTT and clone formation assay and cell cycle and apoptosis by flow cytometry. The levels of miR-144 and TBX1 in H9c2 cells were assessed by qRT-PCR. Dual luciferase reporter assay was used to validate the direct targeting of TBX1 with miR-144. The protein expression levels of TBX1 and its downstream proteins were measured by Western blot analysis. miR-144 inhibited H9c2 cell proliferation by arresting cells in G1 phase. Furthermore, miR-144 induced H9c2 cell apoptosis and activated the JAK2/STAT1 signaling pathway. Bioinformatic predictions and luciferase reporter assay showed that miR-144 directly targets TBX1. Co-overexpression of miR-144 and TBX1 upregulated cell proliferation by accelerating G1 to S phase transition and downregulated cell apoptosis through inhibiting the JAK2/STAT1 signaling pathway. miR-144 acts as a proliferation inhibitor in cardiomyocytes via the TBX1/JAK2/STAT1 axis and is therefore a potential novel therapeutic target for CHD treatment.

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MiR-218 Promotes Adriamycin-Induced H9C2 Apoptosis by Inhibiting Stress-Associated Endoplasmic Reticulum Protein 1

Disease Markers ◽

10.1155/2022/6881103 ◽

2022 ◽

Vol 2022 ◽

pp. 1-10

Author(s):

Qinghua Chen ◽

Gang Chen ◽

Shuofang Zhao

Keyword(s):

Signaling Pathway ◽

P38 Mapk ◽

Cell Apoptosis ◽

Cell Activity ◽

Mapk Signaling ◽

Luciferase Reporter ◽

Tunel Staining ◽

H9c2 Cell ◽

H9c2 Cells ◽

Gene Assay

Objective. Adriamycin is a clinically important chemotherapeutic drug, but its use is restricted due to its myocardial toxicity. Therefore, it is especially important to explore the toxicity mechanism of Adriamycin (ADR) to cardiomyocytes. Methods. The myocardial toxicity model of ADR was constructed in vitro, and the effect of miR-218 inhibitor and sh-Serp1 on the activity of H9C2 cells induced by ADR was detected by MTT method. Also, flow cytometry, real-time polymerase chain reaction (RT-PCR), and TUNEL staining were used to detect the cell apoptosis. The activity of LDH was detected by colorimetry, and the interaction of miR-218 with Serp1 was detected by double-luciferase reporter gene assay. Western blotting technique was used to detect the expression level of caspase3 and p38 MAPK signal pathway. Results. miR-218 inhibitor can obviously inhibit ADR-induced decrease in cell activity of H9C2 cells, inhibit cell apoptosis, and inhibit p38 MAPK signaling pathway activation. Conversely, sh-Serp1 aggravated the decrease in H9C2 cell activity and promoted cell apoptosis. Conclusion. Upregulation of miR-218 expression will promote ADR-induced apoptosis of H9C2 cells. At the same time, we confirmed that the mechanism by which miR-218 promotes myocardial apoptosis was through the Serp1/p38 MAPK/caspase-3 signaling pathway.

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