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We conclude that cardiomyocytes experience epigenetic and transcriptional decline of cardiac gene expression right after birth, contributing to a transition state of CMs at postnatal day 7 that was essential for CM subtype specification during heart maturation. Our results show that CM state transition as a key event in postnatal heart maturation, not only providing insight into heart maturation's molecular foundations, but also opens the door to altering cardiomyocyte fate in disease and regenerative medicine.
Source link: https://doi.org/10.1007/s13238-022-00908-4
In AF, we observed the implicit mechanism of exosomes-miR-148a formation from bone marrow mesenchymal stem cells. The first AF cell and mice models were developed. Cell viability was determined by MTT assays, which were used to determine cell viability of cells by cell viability. Cell apoptosis was detected by cell apoptosis by Flow cytometric analysis and TUNEL analysis. SMOC2 was a miR-148a target gene and triggered apoptosis of HL-1 cells by apoptosis. In addition, miR-148a mimics decreased cell apoptosis, eliminated SMOC2 expression, and raised Bcl-2 expression in AF-treated cells. MiR-148a was overexpressed in BMSC-exosomes, hindering SMOC2 indefinitely, contributing to apoptosis by limiting SMOC2.
Source link: https://doi.org/10.1007/s12033-022-00487-z
MiRNAu2013target gene interactions play a key role in fine-tuning the genetic blueprint governing cardiac maturation, and may reveal critical pathways to be targeted. Methods We analyzed a hiPSC-CM public database to find time-regulated miRNA-u2013target gene interactions based on three logical steps of filtering. In three cell clones, we then introduced miRNA mimics from top eight miRNAs candidates to assess their effect on different aspects of cardiac specification and maturation, including proliferation, sarcomere structure, contractility, and calcium handling. Results We discovered 324 interactions between 29 differentially expressed genes and 51 miRNAs from 20,543 transcripts through to 120 days of hiPSC-CM differentiation, as well as selected 16 genes and 25 miRNAs based on the inverse pattern of expression and consistency in various datasets. We also demonstrated that miR-124 plays a role in Ca2+ handling, with Ca2+ handling evolving characteristics associated with hiPSC-CMs maturation.
Source link: https://doi.org/10.1186/s13287-022-03138-x
Heart disease is one of the heart wall diseases that result in permanent heart wall damage, leading to heart failure. Cellular therapy may help to repair the damaged myocardium. Single cells isolated from an excess heart tissue obtained from the correct ventricular hypertrophy in patients with Tetralogy of Fallot were investigated as part of the future heart study. Cell density from the 500 mg group was 4,867 cells, much higher than the 1,000 mg group; the 590 cell weight was 561 u00b1 490 cells. mgu22121 tissue weight remained 4,867 cells, much higher than the 1,000 mg group; the cell density was 499 cells in the 500 mg group was 4. 867 u00b1 899 cells; Conclusion: Cardiomyocytes isolated from the wasted heart tissue can be a candidate for cardiovascular disease research in the heart because it contained up to 13. 38% cardiomyocytes and 32. 25% of cardiac progenitor cells. Moreover, less than 500 grams of tissue mass may be considered as appropriate, particularly when cardiac cell therapy uses autologous cardiomyocytes.
Source link: https://doi.org/10.1007/s10561-021-09970-4
Cardiomyocytes have been isolated from various stem cells, including human embryonic stem cells and induced pluripotent stem cells, but mature cardiomyocytes are difficult to produce mature cardiomyocytes. We demonstrated that rat hair-follicle-associated pluripotent stem cells had pluripotency and produced mature beating cardiomyocyte sheets distinguishing from rat HAP stem cells. In 10% FBS DMEM and stained with antibodies of the ectoderm, mesoderm, and endoderm type, multiple cell types were demonstrated. The cardiovascular myocytes are distinguished from HAP stem cells' HAP stem cells, showing that they may have medical potential for heart transplantation.
Source link: https://doi.org/10.1007/s00795-022-00322-z
Although the myocardium's physical environment has a significant influence on cardiomyocyte structure and function, myocardiocyte composition and function remains unclear, an analysis of the cardiomyocyte responses to extracellular stiffening remains incomplete. In the absence of cell-u2013cell interactions, we therefore used a cell culture substrate with tunable stiffness to characterize the cardiomyocyte responses to clinically relevant stiffness increases. In the presence of extracellular substrate stiffening, we found that knockdown of Vash2 was sufficient to maintain contractile integrity as well as calcium transient properties.
Source link: https://doi.org/10.1007/s00395-022-00952-5
Objectives Doxorubicin is a type of antitumor drug that is safe, but it can cause cardiomyocyte damage. Following the application of gain- or loss-of-function assays, mouse cardiomyocytes, HL-1 cells, were induced with l u00b5M DOX. HMOX1 and CTGF were highly expressed in DOX-induced mice and correlated with each other, according to a bioinformatics review. HMOX1 and CTGF expression in HL-1 cells after DOX treatment was also elevated after DOX administration, as well as a decrease in cell viability and GSH/GPX4 expression, an increase in ROS levels, apoptosis, and Fe2+ contents, along with a clear decrease in mitochondrial membrane potential dysfunction or loss. However, CTGF overexpression counteracted the effect of HMOX1 silencing on DOX-induced HL-1 cells' viability, apoptosis, ferroptosis, and mitochondrial dysfunction. Conclusions In conclusion, HMOX1 silencing reduced CTGF expression to reduce DOX-induced inflammation, mitochondrial dysfunction, and mouse cardiomyocyte ferroptosis.
Source link: https://doi.org/10.1007/s11748-022-01867-7
Our results We find that in all sema3fb mRNA is expressed by all cardiomyocytes, but ventricular cardiomyocytes secretly express a known receptor Plexina3. In sema3fb CRISPR zebrafish mutants, heart chamber formation is stunted; mutant atria and ventricles are smaller in size than their wild type siblings, likely due to differences in cell size and not cell counts. An examination of chamber specific gene expression at the border between the ventricular and atrial chambers shows deficiencies in chamber specific gene expression at the ventricular chambers' interior, spilling of ventricular chamber genes into the atrium, vice versa, and vice versa, as well as a failure to limit specialized cardiomyocyte markers to the atrioventricular canal. The hypoplastic heart chambers have been attributed to reduced cardiac output and heart edema.
Source link: https://doi.org/10.1186/s12964-022-00874-8
Doxorubicin, an affordable and widely used drug for human malignancy treatment, is widely used in clinical trials, but clinical use is limited due to side effects, particularly cardiotoxicity. DOX can cause apoptosis in cardiomyocytes, according to our current research. In vitro and in vivo, overexpression of lncRNA NONMMUT015745 could reduce DOX-induced cardiomyocyte apoptosis. Rab2A's Ser 33 cytologically interacts with p53 and phosphorylated p53, which in turn promotes phosphorylation, triggering the apoptotic pathway. Our results indicate that lnc5745 protects against DOX-induced cardiomyocyte apoptosis by suppressing Rab2A expression, reducing phosphorylation, and possibly controlling the p53-related apoptotic signalling pathway.
Source link: https://doi.org/10.1038/s41420-022-01144-9
A mouse model of maternal hyperglycemia's embryonic heart tissues from a mouse model of maternal hyperglycemia give further insight into how matHG disrupts heart formation and disrupts second heart field derived cardiomyocyte differentiation. In this research, we used an established murine model of pregestational diabetes to determine transcriptional profiles in key cell-types of the newborn heart exposed to maternal hyperglycemia. Here we show that matHG elicits a variety of physiological responses in E9. 5 and E11. 5 embryonic hearts relative to non-diabetic hearts by single-cell RNA sequencing. MatHG-mediated transcriptional changes in a second heart field lineage that raise CHD risk by altering Isl1-GRN during cardiomyocyte differentiation is shown by our results. A broader effect on understanding the mechanisms of matHG-induced risk of CHD in diabetic pregnancies will be available from gene-environment interactions targeting the Isl1-GRN in cardiac progenitor cells.
Source link: https://doi.org/10.1038/s42003-022-03779-x
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