ArticleExperimental biology and medicine (Maywood, N.J.)2022
The effects of β-catenin on cardiomyogenesis via Islet-1 and MLIP ubiquitination.
Article in Experimental biology and medicine (Maywood, N.J.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed, 1 citations in OpenAlex.
- Nkx2.5: a crucial regulator of cardiac development, regeneration and diseases.Frontiers in cardiovascular medicine · 2023Review
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10 authors at 1 institution in 1 country.
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Abstract
Mesenchymal stem cells (MSCs) can treat myocardial injury-related diseases by differentiating into cardiomyocytes. Islet-1 plays an essential role in cardiac maturation. We have discovered that Islet-1 plays a crucial role in the histone acetylation regulation in this process. In addition, to increase GATA4/Nkx2.5 expression, Islet-1 may bind to Gcn5 and then guide Gcn5 to the GATA4/Nkx2.5 promoters, thereby facilitating the differentiation of MSCs into cardiomyocytes. Islet-1 is an important factor in the maturation of the heart. We have previously found that the pivotal factor in histone acetylation regulation in this process is Islet-1. Furthermore, Islet-1 and Gcn5 may boost GATA4/Nkx2.5 expression, which in turn promotes cardiomyocyte differentiation from MSCs. But the molecular mechanism of Islet-1 binding to GCN5 has not been elucidated. In this study, we found that the competitive binding relationship between Islet-1 and MLIP and GCN5 affected myocardial differentiation. The key enzymes of ubiquitination modification of MLIP and Islet-1 are UBE3C and WWP1, respectively. When short hairpin RNA (shRNA) was used to inhibit β-catenin expression, we found that the expression of UBE3C was upregulated, modifying MLIP ubiquitination and reducing its expression, and it upregulated Islet-1 by inhibiting the expression of WWP1. By using the chromatin immunoprecipitation (ChIP) and luciferase reporter system, we found that when MLIP binds to Islet-1, it significantly inhibits the transcriptional activity of Islet-1. In summary, our results show that decreasing β-catenin regulates the ubiquitination of Islet-1 and MLIP, affecting their expression, reducing the amount of Islet-1 binding to MLIP, and increasing the amount of binding to GCN5 in the nucleus. Therefore, the transcriptional activity of Islet-1 is significantly activated, inducing C3H10T1/2 cells to differentiate into myocytes. Further knowledge of biochemical pathways, including molecular signaling pathways, can provide more insights into the myocardial differentiation mechanism of MSCs.
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