scholarly journals SARS-CoV-2 infection of human iPSC-derived cardiac cells predicts novel cytopathic features in hearts of COVID-19 patients

2020 ◽  
Author(s):  
Juan A. Pérez-Bermejo ◽  
Serah Kang ◽  
Sarah J. Rockwood ◽  
Camille R. Simoneau ◽  
David A. Joy ◽  
...  
Keyword(s):  
Nuclear Dna ◽  
Distinct Pattern ◽  
Cardiac Cells ◽  
Productive Infection ◽  
Heart Cells ◽  
Cardiac Damage ◽  
Autopsy Specimens ◽  
Human Ipsc ◽  
Human Autopsy

ABSTRACTAlthough COVID-19 causes cardiac dysfunction in up to 25% of patients, its pathogenesis remains unclear. Exposure of human iPSC-derived heart cells to SARS-CoV-2 revealed productive infection and robust transcriptomic and morphological signatures of damage, particularly in cardiomyocytes. Transcriptomic disruption of structural proteins corroborated adverse morphologic features, which included a distinct pattern of myofibrillar fragmentation and numerous iPSC-cardiomyocytes lacking nuclear DNA. Human autopsy specimens from COVID-19 patients displayed similar sarcomeric disruption, as well as cardiomyocytes without DNA staining. These striking cytopathic features provide new insights into SARS-CoV-2 induced cardiac damage, offer a platform for discovery of potential therapeutics, and raise serious concerns about the long-term consequences of COVID-19.

scholarly journals SARS-CoV-2 infection of human iPSC-derived cardiac cells reflects cytopathic features in hearts of patients with COVID-19

2021 ◽  
pp. eabf7872
Author(s):  
Juan A. Perez-Bermejo ◽  
Serah Kang ◽  
Sarah J. Rockwood ◽  
Camille R. Simoneau ◽  
David A. Joy ◽  
...  
Keyword(s):  
Induced Pluripotent Stem Cell ◽  
Distinct Pattern ◽  
Cardiac Cells ◽  
Productive Infection ◽  
Heart Cells ◽  
Cardiac Damage ◽  
Autopsy Specimens ◽  
Induced Pluripotent ◽  
Human Ipsc

Although coronavirus disease 2019 (COVID-19) causes cardiac dysfunction in up to 25% of patients, its pathogenesis remains unclear. Exposure of human induced pluripotent stem cell (iPSC)-derived heart cells to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) revealed productive infection and robust transcriptomic and morphological signatures of damage, particularly in cardiomyocytes. Transcriptomic disruption of structural genes corroborates adverse morphologic features, which included a distinct pattern of myofibrillar fragmentation and nuclear disruption. Human autopsy specimens from patients with COVID-19 reflected similar alterations, particularly sarcomeric fragmentation. These striking cytopathic features in cardiomyocytes provide insights into SARS-CoV-2-induced cardiac damage, offer a platform for discovery of potential therapeutics, and raise concerns about the long-term consequences of COVID-19 in asymptomatic as well as severe cases.

Confocal imaging of calcium in intact ventricular muscle provides a new view of excitation-contraction coupling

1996 ◽  
Vol 54 ◽  
pp. 738-739
Author(s):  
W.G. Wier
Keyword(s):  
Local Control ◽  
Cardiac Tissue ◽  
Cell Function ◽  
Isolated Heart ◽  
Cardiac Cells ◽  
Confocal Imaging ◽  
Ion Concentration ◽  
Heart Cell ◽  
Free Calcium ◽  
Heart Cells

A fundamentally new understanding of cardiac excitation-contraction (E-C) coupling is being developed from recent experimental work using confocal microscopy of single isolated heart cells. In particular, the transient change in intracellular free calcium ion concentration ([Ca2+]i transient) that activates muscle contraction is now viewed as resulting from the spatial and temporal summation of small (∼ 8 μm3), subcellular, stereotyped ‘local [Ca2+]i-transients' or, as they have been called, ‘calcium sparks'. This new understanding may be called ‘local control of E-C coupling'. The relevance to normal heart cell function of ‘local control, theory and the recent confocal data on spontaneous Ca2+ ‘sparks', and on electrically evoked local [Ca2+]i-transients has been unknown however, because the previous studies were all conducted on slack, internally perfused, single, enzymatically dissociated cardiac cells, at room temperature, usually with Cs+ replacing K+, and often in the presence of Ca2-channel blockers. The present work was undertaken to establish whether or not the concepts derived from these studies are in fact relevant to normal cardiac tissue under physiological conditions, by attempting to record local [Ca2+]i-transients, sparks (and Ca2+ waves) in intact, multi-cellular cardiac tissue.

UPDATE ON CARDIOVASCULAR IMPLICATIONS OF COVID 19

2021 ◽  
pp. 238-242
Author(s):  
Pradeep Kumar Radhakrishnan ◽  
Gayathri Ananyajyothi Ambat ◽  
Roshini Ambat ◽  
Syed Ilas Basha ◽  
Hema Prakash ◽  
...  
Keyword(s):  
Virus Disease ◽  
Systemic Vasculitis ◽  
Myocardial Damage ◽  
Viral Disease ◽  
Cardiac Damage ◽  
Corona Virus ◽  
Global Pandemic ◽  
Acute Myocardial Injury ◽  
Exercise Induced

On March 11 2020 WHO declares corona viral disease as a global pandemic .COVID 19 pandemic has taken the world by storm and many countries like India is now experiencing a second surge due to mutant strains. Global health emergency has been precipitated by this corona virus disease caused by SARS CoV2.Acute and intermediate effects on cardiovascular system are becoming obvious with progression of time. SARS-CoV-2-related endothelial dysfunction results in an augmented risk for venous thromboembolism, systemic vasculitis, endothelial cell apoptosis, and inammation in various organs. Acute infections have troponin elevation more due to indirect cardiac damage though denite patterns of direct damage do exist. Intermediate evaluation in patients with resolved infections shows increased incidence of exercise induced arrhythmias and residual cardiovascular symptoms. The virus with its zoonotic origin based upon its genomic identity to bat derived SARS corona virus has a human to human transmission mode.ACE 2 receptors facilitate cellular entry and has been implicated in direct and indirect myocardial damage. Myocarditis, acute myocardial injury, arrhythmias and thromboembolism dominates the clinical picture. Role of imaging must be dened in relation to relevant clinical ndings. With arrival of vaccine and widespread vaccination global programs, we can look forward to understanding and managing long term complications of this disease. Prognostic implications of a resolved disease need to be evaluated by future studies.

scholarly journals Medium- to long-term survival and functional examination of human iPSC-derived retinas in rat and primate models of retinal degeneration

EBioMedicine ◽  
2019 ◽  
Vol 39 ◽  
pp. 562-574 ◽  
Author(s):  
Hung-Ya Tu ◽  
Takehito Watanabe ◽  
Hiroshi Shirai ◽  
Suguru Yamasaki ◽  
Masaharu Kinoshita ◽  
...  
Keyword(s):  
Retinal Degeneration ◽  
Term Survival ◽  
Long Term Survival ◽  
Human Ipsc ◽  
Functional Examination

scholarly journals 5-bromo-2'-deoxyuridine-stimulated calcium ion- or magnesium ion-dependent ecto-(adenosine triphosphatase) activity of cultured hamster cardiac cells

1977 ◽  
Vol 164 (3) ◽  
pp. 645-652 ◽  
Author(s):  
G A Coetzee ◽  
W Gevers
Keyword(s):  
Adenosine Triphosphatase ◽  
Primary Cultures ◽  
Cardiac Cells ◽  
Cell Protein ◽  
Heart Cells ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Active Centre ◽  
Cellular Dna ◽  
Hamster Heart

1. Treatment of hamster heart cells in primary culture with 5-bromo-2'-deoxyuridine resulted in the greatly increased activity of a particulate Ca2+- or Mg2+-dependent ATPase (adenosine triphosphatase). 2. 5-Bromo-2'-deoxyuridine exerted these effects only when it was incorporated into cellular DNA, and then in a concentration-dependent manner. 3. Serially replated cells contained less of the activity (expressed as a function of total cell protein) than did the primary cultures, but the stimulation caused by 5-bromo-2'-deoxyuridine addition was much greater. 4. The affected enzyme was apparently localized in the plasma membrane of the cells with its active centre exposed to the outer environment [ecto-(ATPase) dependent on Ca2+ or Mg2+].5. The activity was unaffected by treatment with p-chloromercuriphenylsulphonate, ouabain andverapamil. 6. Ecto (5'-nucleotidase) activity was not increased by 5-bromo-2'-deoxyuridine treatment of cells, and ecto-(p-nitrophenyl phosphatase) activity was only slightly enhanced.

scholarly journals Reproducibility of Molecular Phenotypes after Long-Term Differentiation to Human iPSC-Derived Neurons: A Multi-Site Omics Study

2018 ◽  
Vol 11 (4) ◽  
pp. 897-911 ◽  
Author(s):  
Viola Volpato ◽  
James Smith ◽  
Cynthia Sandor ◽  
Janina S. Ried ◽  
Anna Baud ◽  
...  
Keyword(s):  
Molecular Phenotypes ◽  
Human Ipsc

Characterization of a novel subset of cardiac cells and their progenitors in the Drosophila embryo

Development ◽  
2000 ◽  
Vol 127 (22) ◽  
pp. 4959-4969 ◽  
Author(s):  
E.J. Ward ◽  
J.B. Skeath
Keyword(s):  
Heart Development ◽  
Cell Types ◽  
Cardiac Cells ◽  
Lineage Tracing ◽  
Drosophila Embryo ◽  
Heart Cells ◽  
Pericardial Cells ◽  
Asymmetric Divisions ◽  
Genetic Mechanisms

The Drosophila heart is a simple organ composed of two major cell types: cardioblasts, which form the simple contractile tube of the heart, and pericardial cells, which flank the cardioblasts. A complete understanding of Drosophila heart development requires the identification of all cell types that comprise the heart and the elucidation of the cellular and genetic mechanisms that regulate the development of these cells. Here, we report the identification of a new population of heart cells: the Odd skipped-positive pericardial cells (Odd-pericardial cells). We have used descriptive, lineage tracing and genetic assays to clarify the cellular and genetic mechanisms that control the development of Odd-pericardial cells. Odd skipped marks a population of four pericardial cells per hemisegment that are distinct from previously identified heart cells. We demonstrate that within a hemisegment, Odd-pericardial cells develop from three heart progenitors and that these heart progenitors arise in multiple anteroposterior locations within the dorsal mesoderm. Two of these progenitors divide asymmetrically such that each produces a two-cell mixed-lineage clone of one Odd-pericardial cell and one cardioblast. The third progenitor divides symmetrically to produce two Odd-pericardial cells. All remaining cardioblasts in a hemisegment arise from two cardioblast progenitors each of which produces two cardioblasts. Furthermore, we demonstrate that numb and sanpodo mediate the asymmetric divisions of the two mixed-lineage heart progenitors noted above.

scholarly journals A Review of Accelerated Long-Term Forgetting in Epilepsy

2020 ◽  
Vol 10 (12) ◽  
pp. 945
Author(s):  
Rūta Mameniškienė ◽  
Kristijonas Puteikis ◽  
Arminas Jasionis ◽  
Dalius Jatužis
Keyword(s):  
Memory Consolidation ◽  
Epileptiform Activity ◽  
Distinct Pattern ◽  
Imaging Data ◽  
Novel Studies ◽  
Memory Disorder ◽  
Antiepileptic Medication ◽  
Reported Data ◽  
Neocortical Network

Accelerated long-term forgetting (ALF) is a memory disorder that manifests by a distinct pattern of normal memory for up to an hour after learning, but an increased rate of forgetting during the subsequent hours and days. The topic of ALF has gained much attention in group studies with epilepsy patients and the phenomenon has been shown to have contradictory associations with seizures, epileptiform activity, imaging data, sleep, and antiepileptic medication. The aim of this review was to explore how clinical and imaging data could help determine the topographic and physiological substrate of ALF, and what is the possible use of this information in the clinical setting. We have reviewed 51 group studies in English to provide a synthesis of the existing findings concerning ALF in epilepsy. Analysis of recently reported data among patients with temporal lobe epilepsy, transient epileptic amnesia, and generalized and extratemporal epilepsies provided further indication that ALF is likely a disorder of late memory consolidation. The spatial substrate of ALF might be located along the parts of the hippocampal–neocortical network and novel studies reveal the increasingly possible importance of damage in extrahippocampal sites. Further research is needed to explore the mechanisms of cellular impairment in ALF and to develop effective methods of care for patients with the disorder.

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