Characterization of contracting cardiomyocyte colonies in the primary culture of neonatal rat myocardial cells: A model of in vitro cardiomyogenesis

Belostotskaya, G. B.; Golovanova, T. A.

doi:10.4161/cc.27768

Cited by 22 publications

(23 citation statements)

References 34 publications

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“…Mouse neonatal hearts were enzymatically dissociated into a single cell suspension, as previously described [27]. Briefly, the hearts were finely cut and broken up into single cells in 0.1% collagenase/ dispace (Roche).…”

Section: Methodsmentioning

confidence: 99%

MiR-126 Affects Brain-Heart Interaction after Cerebral Ischemic Stroke

Chen

Cui

Yang

et al. 2017

Transl. Stroke Res.

132

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Cardiovascular diseases are approximately three times higher in patients with neurological deficits than in patients without neurological deficits. MicroRNA-126 (MiR-126) facilitates vascular remodeling and decreases fibrosis and is emerging as an important factor in the pathogenesis of cardiovascular diseases and cerebral stroke. In this study, we tested the hypothesis that decreased miR-126 after ischemic stroke may play an important role in regulating cardiac function. Wild-type (WT), specific conditional-knockout endothelial cell miR-126 (miR-126EC−/−), and miR-126 knockout control (miR-126fl/fl) mice were subjected to distal middle cerebral artery occlusion (dMCAo) (n = 10/group). Cardiac hemodynamics and function were measured using transthoracic Doppler echocardiography. Mice were sacrificed at 28 days after dMCAo. WT mice subjected to stroke exhibited significantly decreased cardiac ejection fraction and increased myocyte hypertrophy, fibrosis as well as increased heart inflammation, infiltrating macrophages, and oxidative stress compared to non-stroke animals. Stroke significantly decreased serum and heart miR-126 expression and increased miR-126 target genes, vascular cell adhesion protein-1, and monocyte chemotactic protein-1 gene, and protein expression in the heart compared to non-stroke mice. MiR-126EC−/− mice exhibited significantly decreased cardiac function and increased cardiomyocyte hypertrophy, fibrosis, and inflammatory factor expression after stroke compared to miR-126fl/fl stroke mice. Exosomes derived from endothelial cells of miR-126EC−/− (miR-126EC−/−EC-Exo) mice exhibited significantly decreased miR-126 expression than exosomes derived from miR-126fl/fl (miR-126fl/fl-EC-Exo) mice. Treatment of cardiomyocytes subjected to oxygen glucose deprivation with miR-126fl/fl-EC-Exo exhibited significantly decreased hypertrophy than with miR-126EC−/−EC-Exo treatment. Ischemic stroke directly induces cardiac dysfunction. Decreasing miR-126 expression may contribute to cardiac dysfunction after stroke in mice.

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Section: Methodsmentioning

confidence: 99%

MiR-126 Affects Brain-Heart Interaction after Cerebral Ischemic Stroke

Chen

Cui

Yang

et al. 2017

Transl. Stroke Res.

132

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“…In vitro culture of neonatal rat cardiomyocytes was performed as described previously 13. Briefly, Wister rats aged 2 to 3 days were anesthetized and decapitated.…”

Section: Methodsmentioning

confidence: 99%

“…In vitro culture of neonatal rat cardiomyocytes was performed as described previously. 13 Briefly, Wister rats aged 2 to 3 days were anesthetized and decapitated. The hearts were minced and dissociated with 0.25% trypsinase (Sigma-Aldrich) in an incubator with 5% CO 2 at 37°C for 15 minutes.…”

Section: Culture Of Neonatal and Embryonic Rat Cardiomyocytesmentioning

confidence: 99%

Mitogen‐Activated Protein Kinase and Intracellular Polyamine Signaling Is Involved in TRPV1 Activation–Induced Cardiac Hypertrophy

Chen

Xin

Liu

et al. 2016

JAHA

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BackgroundThe transient receptor potential vanilloid type 1 (TRPV1) is expressed in the cardiovascular system, and increased TRPV1 expression has been associated with cardiac hypertrophy. Nevertheless, the role of TRPV1 in the pathogenesis of cardiac hypertrophy and the underlying molecular mechanisms remain unclear.Methods and ResultsIn cultured cardiomyocytes, activation of TRPV1 increased cell size and elevated expression of atrial natriuretic peptide mRNA and intracellular calcium level, which was reversed by TRPV1 antagonist capsazepine. Increased expression of phosphorylated calmodulin‐dependent protein kinase IIδ and mitogen‐activated protein kinases were found in TRPV1 agonist capsaicin‐treated cardiomyocytes. Selective inhibitor of calmodulin‐dependent protein kinase IIδ decreased phosphorylation of extracellular signal–regulated kinases and p38. Capsaicin induced an increase in expression of ornithine decarboxylase protein, which is the key enzyme in polyamine biosynthesis in cardiomyocytes. Nevertheless, there was no obvious change of ornithine decarboxylase expression in TRPV1 knockdown cells after capsaicin treatment, and specific inhibitors of calmodulin‐dependent protein kinase IIδ or p38 downregulated the capsaicin‐induced expression of ornithine decarboxylase. Capsazepine alleviated the increase in cross‐sectional area of cardiomyocytes and the ratio of heart weight to body weight and improved cardiac function, including left ventricular internal end‐diastolic and ‐systolic dimensions and ejection fraction and fractional shortening percentages, in mice treated with transverse aorta constriction. Capsazepine also reduced expression of ornithine decarboxylase and cardiac polyamine levels. Transverse aorta constriction induced increases in phosphorylated calmodulin‐dependent protein kinase IIδ and extracellular signal–regulated kinases, and p38 and Serca2a were attenuated by capsazepine treatment.ConclusionsThis study revealed that the mitogen‐activated protein kinase signaling pathway and intracellular polyamines are essential for TRPV1 activation–induced cardiac hypertrophy.

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“…Lastly, we utilized neonatal ventricular CMs isolated from 2-day old rats for our study, which are able to transition from neonatal to mature electrophysiological state, featuring well-expression of Cx43 electrical gap junctions, stable membrane resting potential, and enhanced depolarization amplitude. [68][69][70] Such intrinsic (i.e. native) cellular properties may shield the potential impact of scaffold conductivity on excitability and synchronicity of the engineered tissue.…”

Section: Influence Of Hydrogel Matrix Characteristics On Electrical Ementioning

confidence: 99%

The influence of electrically conductive and non-conductive nanocomposite scaffolds on the maturation and excitability of engineered cardiac tissues

et al. 2019

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Characterization of contracting cardiomyocyte colonies in the primary culture of neonatal rat myocardial cells: A model of in vitro cardiomyogenesis

Cited by 22 publications

References 34 publications

MiR-126 Affects Brain-Heart Interaction after Cerebral Ischemic Stroke

MiR-126 Affects Brain-Heart Interaction after Cerebral Ischemic Stroke

Mitogen‐Activated Protein Kinase and Intracellular Polyamine Signaling Is Involved in TRPV1 Activation–Induced Cardiac Hypertrophy

The influence of electrically conductive and non-conductive nanocomposite scaffolds on the maturation and excitability of engineered cardiac tissues

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