ArticleEvidence-based complementary and alternative medicine : eCAM2021
miR-16-5p Regulates PTPN4 and Affects Cardiomyocyte Apoptosis and Autophagy Induced by Hypoxia/Reoxygenation.
Article in Evidence-based complementary and alternative medicine : eCAM, 2021. 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.
- Unraveling Optimal Dose and Responsive Markers for Human Cord Blood Derived Mononuclear Cells in Alleviating Bronchopulmonary Dysplasia in Neonatal Mice.International journal of stem cells · 2025Article
- Colonization withbioRxiv : the preprint server for biology · 2025Article
- Long-term impact of anthracycline in early-stage breast cancer, bridging of MiRNAs profiler for early cardiotoxicity.Cardio-oncology (London, England) · 2025Article
- Comprehensive evaluation of non-coding RNA-mediated autophagy regulation in myocardial ischemia-reperfusion injury.Frontiers in pharmacology · 2025Review
- miR-16-5p aggravates sepsis-associated acute kidney injury by inducing apoptosis.Renal failure · 2024Article
- Crosstalk between myocardial autophagy and sterile inflammation in the development of heart failure.Autophagy reports · 2024Review
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Authors and funding
4 authors.
Funding
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Abstract
objectivesTo explore the effects of miR-16-5p and PTPN4 on the apoptosis and autophagy of AC16 cardiomyocytes after hypoxia/reoxygenation treatment.
methodsAC16 cells were divided into the control group (NC), hypoxia/reoxygenation group (H/R), knockdown miR-16-5p negative control group (NC inhibitor), knockdown miR-16-5p group (miR-16-5p inhibitor), overexpression miR-16-5p negative control group (NC mimics), overexpression miR-16-5p group (miR-16-5p mimics), silent PTPN4 negative control group (sh-NC), silent PTPN4 group (sh-PTPN4), and silent PTPN4 + knockdown miR-16-5p group (sh-PTPN4 + miR-16-5p inhibitor). Real-time fluorescent quantitative PCR (RT-qPCR) and western blotting (WB) were used to measure the expression level of miR-16-3p, miR-16-5p, protein tyrosine phosphatase nonreceptor type 4 (PTPN4), and autophagy-related proteins (beclin-1, LC3 II/I, and P26) in AC16 cells. The apoptosis level of AC16 cells in each group was measured by flow cytometry and TUNEL. The dual-luciferase reporter gene experiment was also used to verify the targeting relationship between miR-16-5p and PTPN4.
resultsAfter H/R treatment, the levels of myocardial injury markers including LDH and CK-MB in AC16 cells were increased significantly (
conclusionsThe expression of miR-16-5p is upregulated in AC16 cells after H/R treatment and the knockdown which can protect AC16 cells from H/R-induced cell damage that may be due to its regulation on the expression of PTPN4.
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Registered trials
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