ArticleMolecular medicine reports2019
Downregulation of miR‑16 protects H9c2(2‑1) cells against hypoxia/reoxygenation damage by targeting CIAPIN1 and regulating the NF‑κB pathway.
Article in Molecular medicine reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- Circulating microRNAs Showed Specific Responses according to Metabolic Syndrome Components and Sex of Adults from a Population-Based Study.Metabolites · 2022Article
- miR-16-5p Suppression Protects Human Cardiomyocytes against Endoplasmic Reticulum and Oxidative Stress-Induced Injury.International journal of molecular sciences · 2022Article
- Tat-CIAPIN1 protein prevents against cytokine-induced cytotoxicity in pancreatic RINm5F β-cells.BMB reports · 2021Article
- miR-362-3p Targets Orosomucoid 1 to Promote Cell Proliferation, Restrain Cell Apoptosis and Thereby Mitigate Hypoxia/Reoxygenation-Induced Cardiomyocytes Injury.Cardiovascular toxicology · 2021Article
- Preeclamptic Women Have Disrupted Placental microRNA Expression at the Time of Preeclampsia Diagnosis: Meta-Analysis.Frontiers in bioengineering and biotechnology · 2021Review
- A Roadmap for Fixing the Heart: RNA Regulatory Networks in Cardiac Disease.Molecular therapy. Nucleic acids · 2020Review
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of the present study was to determine the function of microRNA‑16 (miR‑16) in myocardial hypoxia/reoxygenation (H/R)‑induced cardiomyocyte injury and the possible mechanism underlying its involvement. An H/R model was constructed using H9c2(2‑1) cells in vitro. The results of reverse transcription‑quantitative PCR demonstrated that the expression levels of miR‑16 were significantly upregulated in H9c2(2‑1) cells in the H/R group compared with the sham group (1.53±0.09 vs. 1.0±0.08; P=0.0019). Cell Counting Kit‑8 assays revealed that the relative proliferative ability of H9c2(2‑1) cells was significantly decreased in the H/R + negative control (NC) group compared with the sham group (0.53±0.05 vs. 1.0±0.08; P=0.00005). Upregulation of miR‑16 using miR‑16 mimics further decreased the proliferative ability of cells (0.31±0.03 vs. 0.53±0.05; P=0.0097), whereas downregulation of miR‑16 using an miR‑16 inhibitor increased the proliferative ability of cells compared with the H/R+NC group (0.89±0.08 vs. 0.53±0.05; P=0.000385). Flow cytometric analysis found that the apoptotic rate of H9c2(2‑1) cells was increased significantly following H/R compared with the sham group (25.86±2.62% vs. 9.29±0.82%, P=0.000014). Upregulation of miR‑16 further increased the apoptotic rate (38.62±2.04% vs. 25.86±2.62%; P=0.000099), whereas downregulation of miR‑16 decreased the apoptotic rate compared with the H/R+NC group (15.14±0.92% vs. 25.86±2.62%; P=0.000343). miR‑16 directly bound to the 3'‑untranslated region of cytokine‑induced apoptosis inhibitor 1 (CIAPIN1) and negatively modulated CIAPIN1 expression. Overexpression of CIAPIN1 reversed the changes in the expression of apoptosis‑associated proteins caused by H/R. Western blot analysis revealed that the levels of phospho‑(p‑)nuclear factor‑κB (NF‑κB) and p‑NF‑κB inhibitor α (IκBα) were upregulated following H/R (1.82±0.11 vs. 1.0±0.08; P=0.000152; and 1.77±0.07 vs. 1.0±0.00; P=0.000024, respectively), and these changes were further enhanced when miR‑16 expression levels were increased (3.10±0.14 vs. 1.82±0.11; P=0.000006; and 2.19±0.10 vs. 1.77±0.07; P=0.0017, respectively). Downregulation of miR‑16 exhibited the opposite effect on p‑NF‑κB and p‑IκBα expression levels. The present study illustrates that downregulation of miR‑16 may protect against H/R‑induced injury partially by targeting CIAPIN1 and the NF‑κB signaling pathway.
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