ArticleKorean circulation journal2024
LncRNA PART1 Attenuates Myocardial Ischemia-Reperfusion Injury by Regulating TFAP2C/DUSP5 Axis via miR-302a-3p.
Article in Korean circulation journal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 5 citations in OpenAlex.
- Long Non-Coding RNA PART1 in Alzheimer's Disease: Clinical Value and Improvement of Neurotoxicity and Apoptosis via miR-770-5p.Neurochemical research · 2026Article
- Cellular Responses to Cold Stress in Pampus argenteus: Involvement of Dusp5 in MAPK Signaling, Apoptosis Suppression, and Organelle Protection.Marine biotechnology (New York, N.Y.) · 2026Article
- miR-302a-3p mitigates intervertebral disc degeneration progression through regulating EPHA2.Journal of orthopaedic surgery and research · 2025Article
- Epigenetic Regulation of Regulated Cell Death in Aging-Related Diseases: Clinical Perspectives.Aging and disease · 2025Article
- Cardiovascular diseases in the elderly: possibilities for modulating autophagy using non-coding RNAs.Frontiers in cell and developmental biology · 2025Review
- Comprehensive evaluation of non-coding RNA-mediated autophagy regulation in myocardial ischemia-reperfusion injury.Frontiers in pharmacology · 2025Review
- Cardiomyocyte Autophagy: A Novel Therapeutic Target by LncRNA PART1.Korean circulation journal · 2024Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
BACKGROUND AND
objectivesMyocardial ischemia-reperfusion injury (MIRI) refers to the damage of cardiac function caused by restoration of blood flow perfusion in ischemic myocardium. However, long non-coding RNA prostate androgen regulated transcript 1 (PART1)'s role in MIRI remain unclear.
methodsImmunofluorescence detected LC3 expression. Intermolecular relationships were verified by dual luciferase reporter assay. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, flow cytometry and transferase-mediated dUTP nick-end labeling (TUNEL) assays analyzed cell viability and apoptosis. The release of lactate dehydrogenase was tested via enzyme-linked immunosorbent assay (ELISA). Left anterior descending coronary artery surgery induced a MIRI mouse model. Infarct area was detected by 2,3,5-triphenyltetrazolium chloride staining. Hematoxylin and eosin staining examined myocardial injury. ELISA evaluated myocardial marker (creatine kinase MB) level.
resultsPART1 was decreased in hypoxia/reoxygenation (H/R) induced AC16 cells and MIRI mice. PART1 upregulation attenuated the increased levels of Bax, beclin-1 and the ratio of LC3II/I, and enhanced the decrease of Bcl-2 and p62 expression in H/R-treated cells. PART1 upregulation alleviated H/R-triggered autophagy and apoptosis via miR-302a-3p. Mechanically, PART1 targeted miR-302a-3p to upregulate transcription factor activating enhancer-binding protein 2C (TFAP2C). TFAP2C silencing reversed the protected effects of miR-302a-3p inhibitor on H/R treated AC16 cells. We further established TFAP2C combined to dual-specificity phosphatase 5 (DUSP5) promoter and activated DUSP5. TFAP2C upregulation suppressed H/R-stimulated autophagy and apoptosis through upregulating DUSP5. Overexpressed PART1 reduced myocardial infarction area and attenuated MIRI in mice.
conclusionPART1 improved the autophagy and apoptosis in H/R-exposed AC16 cells through miR-302a-3p/TFAP2C/DUSP5 axis, which might provide novel targets for MIRI treatment.
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