ArticleIn vitro cellular & developmental biology. Animal2018
LncRNA-uc.40 silence promotes P19 embryonic cells differentiation to cardiomyocyte via the PBX1 gene.
Article in In vitro cellular & developmental biology. Animal, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- Long Non-Coding Ribonucleic Acid Taurine Up-Regulated Gene 1 Accelerates Ventricular Septal Defect Formation in Children.Brazilian journal of cardiovascular surgery · 2026Article
- Characterizing and decoding ultraconserved regions uncovers their regulatory significance in human brain development and disorders.Communications biology · 2025Article
- Mechanosensitive lncRNA H19 promotes chondrocyte autophagy, but not pyroptosis, by targeting miR-148a in post-traumatic osteoarthritis.Non-coding RNA research · 2025Article
- The molecular mechanisms of cardiac development and related diseases.Signal transduction and targeted therapy · 2024Review
- The expression profile analysis and functional prediction of lncRNAs in peripheral blood mononuclear cells in maintenance hemodialysis patients developing heart failure.Scientific reports · 2024Article
- Ultra-conserved RNA: a novel biological tool with diagnostic and therapeutic potential.Discover oncology · 2023Review
- Research progress of PBX1 in developmental and regenerative medicine.International journal of medical sciences · 2023Review
- PBX1 attenuates HCell stress & chaperones · 2022Article
- The long non-coding road to endogenous cardiac regeneration.Heart failure reviews · 2019Review
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Uc.40 is a long noncoding RNA that is highly conserved among different species, although its function is unknown. It is highly expressed in abnormal human embryonic heart. We previously reported that overexpression of uc.40 promoted apoptosis and inhibited proliferation of P19 cells, and downregulated PBX1, which was identified as a potential target gene of uc.40. The current study evaluated the effects of uc40-siRNA-44 (siRNA against uc.40) on the differentiation, proliferation, apoptosis, and mitochondrial function in P19 cells, and investigated the relationship between uc.40 and PBX1 in cardiomyocytes. The uc.40 silencing expression was confirmed by quantitative real-time polymerase chain reaction (RT-PCR). Observation of morphological changes in transfected P19 cells during different stages of differentiation revealed that uc40-siRNA-44 increased the number of cardiomyocyes. There was no significant difference in the morphology or time of differentiation between the uc40-siRNA-44 group and the control group. uc40-siRNA-44 significantly promoted proliferation of P19 cells and inhibited serum starvation-induced apoptosis. There was no significant difference in mitochondrial DNA copy number or cellular ATP level between the two groups, and ROS levels were significantly decreased in uc40-siRNA-44-transfected cells. The levels of PBX1 and myocardial markers of differentiation were examined in transfected P19 cells; uc40-siRNA-44 downregulated myocardial markers and upregulated PBX1 expression. These results suggest that uc.40 may play an important role during the differentiation of P19 cells by regulation of PBX1 to promote proliferation and inhibit apoptosis. These studies provide a foundation for further study of uc.40/PBX1 in cardiac development.
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