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Cardiomyocytes - DOAJ

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Last Updated: 10 September 2022

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The protective effects of Clerodendranthus spicatus (Thunb.) C. Y. Wu extract on oxidative stress induced by 2,2'-azo (2-methylpropamidine) dihydrochloride in HL-1 mouse cardiomyocytes

Cell survival rates were determined by the 3--2,5-hydroxypyrogenide assay, and in Dulbecco's Modified Eagle Medium plus AAPH for 4 h, assay. Cell survival rates were determined by chronic cell culture in HL-1 mouse cardiomyocytes induced by 2,2'-oxidation stress, induced by hydroxyl-2H-tetrazolium bromide (Chesterocyte proliferation was determined by continuous cultured cells. The determination of MDA and total reactive oxygen species amounts were determined by thiobarbituric acid colorimetry and the 2',7'-dichlorofluorescent sodium yellow diacetate probe, respectively. The CSTE also elevated the enzyme enzymes' production, as well as the u03b3-GCS and GSH levels in damaged cells. In addition, the CSTE improved the endogenous antioxidant system, thus reducing the oxidative stress caused by AAPH.

Source link: https://doi.org/10.3389/fcvm.2022.984813


Cardiomyocytes: Analysis of Temperature Response and Signal Propagation Between Dissociated Clusters Using Novel Video-Based Movement Analysis Software

Human-induced pluripotent stem cell-derived cardiomyocytes are a good starting point for functional cell and tissue models that can be used in heart research, pharmaceutical industry, and future regenerative medicine. Temperature is a fundamental property, and the acute effect of temperature on hiPSC-CM functions has been investigated previously. Temperature monitoring at the actual cell location is difficult with bulky external sensors; however, a TSP with resistive microsensors provides a quick alternative. With a Q 10 temperature coefficient of 2. 2, experimental findings showed that temperature nonlinearly affects the hiPSC-CM beating frequency. We also present novel findings on the visualization of hiPSC-CM contractile networking and non-invasive image-based monitoring of signal propagation between dissociated CM clusters. In addition, the software can also handle movement center detection and independent estimation of the relaxation and contraction parameters.

Source link: https://doi.org/10.1109/ACCESS.2020.3001191


Bioenergetic and Metabolic Impairments in Induced Pluripotent Stem Cell-Derived Cardiomyocytes Generated from Duchenne Muscular Dystrophy Patients

Mutations in the dystrophin gene and dilated cardiomyopathy are a common cause of morbidity and mortality in DMD patients. DCM is caused by metabolic deficiencies, according to an adult male, an adult male, a 7-year-old male, and a 13-year-old male, all compared to two healthy volunteers. Adult DMD CMs had decreased energy metabolism and abnormal mitochondrial structure and function, which caused diminished energy metabolism and altered mitochondrial structure and function, according to We found that: adult DMD CMs had decreased energy metabolism and decreased mitochondrial structure and function. The 7y CM's were similar to that of healthy CMs, at least in DMD adult CMs. mitochondrial functions were reduced by 58% by 45u201348%, but healthy CMs' regular CMs had similar results. In summary, DMD iPSC-CMs have bioenergetic and metabolic deficiencies that are linked to rhythm disorders corresponding to the patient's phenotype, thereby establishing new target for alleviating cardiomyopathy in DMD patients.

Source link: https://doi.org/10.3390/ijms23179808


MicroRNA Let-7a, -7e and -133a Attenuate Hypoxia-Induced Atrial Fibrosis via Targeting Collagen Expression and the JNK Pathway in HL1 Cardiomyocytes

The primary objective of this research was to investigate the role of micro-ribonucleic acids in the modulation of fibrotic molecular functions in response to hypoxic conditions, which may mediate atrial fibrosis. MiRNA arrays were used to determine the specific miRNAs responsible for fibrotic gene expression under a condition of hypoxia induced by a hypoxia chamber. In vitro, hypoxic atrial cardiac cells, miR-let-7a, miR-let-7e, and miR-133a were discovered to be the direct regulatory targets of miR-let-7a, miR-let-7e, and miR-133a. The expressions of COL1A and COL3A were influenced by miRNA mimicry and antagomir therapy, but hypoxia-induced collagen production was limited by miR-133a, miR-let-7a, or miR-let-7e. COL1A and COL3A were the fibrotic markers fibrotic markers that were not released by the JNK inhibitor SP600125. MiRNA let-7a, miR-let-7e, and miR-133a all play significant roles in hypoxia-related fibrosis by blocking collagen production and post-transcriptional suppression by the JNK pathway.

Source link: https://doi.org/10.3390/ijms23179636


ACTN2 Mutant Causes Proteopathy in Human iPSC-Derived Cardiomyocytes

In comparison to ACTN2wt in 2D-cultured hiPSC-CMs, ACTN2mut showed a higher percentage of multinucleation, protein aggregation, hypertrophy, myofibrillar disarray, and activatement of both the ubiquitin-proteasome system and the autophagy-lysosomal pathway. In conclusion, our report shows that proteolytic enzymes in ACTN2 mutation hiPSC-CMs are able to cope with ACTN2 aggregation and therefore directs toward proteopathy as an additional cellular pathology caused by this ACTN2 variant, which may be related to human ACTN2 -associated cardiomyopathies.

Source link: https://doi.org/10.3390/cells11172745


Assessing Drug-Induced Mitochondrial Toxicity in Cardiomyocytes: Implications for Preclinical Cardiac Safety Evaluation

In a preclinical cardiac safety assessment for over 15 years, comprehensive testing for proarrhythmic risks of drugs has been conducted. Of the cardiovascular adverse-event-related black box warnings issued by the U. S. Food and Drug Administration, mitochondrial impairment is a common form of cardiotoxicity and is believed to account for more than half of cardiovascular adverse-event-related black box warnings. We emphasize the benefits of using adult human primary cardiomyocytes for the analysis of mitochondrial morphology and function, as well as the need for a new cardiac safety testing platform that integrates mitochondrial toxicity and proarrhythmic risk evaluation in cardiac safety evaluation.

Source link: https://doi.org/10.3390/pharmaceutics14071313


Echinochrome A Protects Mitochondrial Function in Cardiomyocytes against Cardiotoxic Drugs

Echinochrome A is a naphthoquinoid pigment from sea urchins that has antioxidant, antimicrobial, anti-inflammatory, and chelating properties. We investigated the protective role of Ech A against toxic agents that cause the death of rat cardiac myoblast H9c2 cells and isolated rat cardiomyocytes in this study. Ech A co-treatment also reduced the effects of these cardiotoxic agents on mitochondrial oxidative phosphorylation and adenosine triphosphate levels. These results show that Ech A's therapeutic potential for minimizing cardiotoxic agent-induced damage.

Source link: https://doi.org/10.3390/md12052922


Decrease in Ca 2+ Concentration in Quail Cardiomyocytes Is Faster than That in Rat Cardiomyocytes

In this study, we compared Ca 2+ concentrations in cardiomyocytes isolated from adult quails and rats to help clarify the mechanism that causes rapid heart rates in birds. The time to peak in quails was statistically longer than in rats when using Fura-2 acetoxymethyl ester. Ca 2+ concentration change in quails was shorter in quails than in rats, as a result. The decrease in Ca 2+ concentration in quail cardiomyocytes was quicker in the center of the cell than near the cell membrane, according to a spatiotemporal study. These results show that avian cardiomyocytes respond rapidly to Ca 2+ removal capacity in the central portion of the cell relative to mammalian cardiomyocytes, and that compared to mammalian cardiomyocytes.

Source link: https://doi.org/10.3390/pr10030508

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions