ArticleJournal of cellular and molecular medicine2009
Re-expression of alpha skeletal actin as a marker for dedifferentiation in cardiac pathologies.
Article in Journal of cellular and molecular medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.
- A systematic review of fetal genes as biomarkers of cardiac hypertrophy in rodent models of diabetes.PloS one · 2014Pooled it
- Loss of Myofibrils in Cardiomyocytes as a Morphological Indicator of Reduced Compensatory Capabilities of Hypertrophied Myocardium.Bulletin of experimental biology and medicine · 2024Article
- Cardiac maturation.Journal of molecular and cellular cardiology · 2024Review
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- The Role of Oncostatin M and Its Receptor Complexes in Cardiomyocyte Protection, Regeneration, and Failure.International journal of molecular sciences · 2022Review
- The Role of Lamins in the Nucleoplasmic Reticulum, a Pleiomorphic Organelle That Enhances Nucleo-Cytoplasmic Interplay.Frontiers in cell and developmental biology · 2022Review
- Kidney Response to Chemotherapy-Induced Heart Failure: mRNA Analysis in Normotensive andInternational journal of molecular sciences · 2021Article
- Cell-to-cell lactate shuttle operates in heart and is important in age-related heart failure.Aging · 2020Article
- Gallic acid improves cardiac dysfunction and fibrosis in pressure overload-induced heart failure.Scientific reports · 2018Article
- Actin isoform expression patterns in adult extracardiac and cardiac rhabdomyomas indicate a different cell of origin.Virchows Archiv : an international journal of pathology · 2017Article
- Article
- Myocardial plasticity: cardiac development, regeneration and disease.Current opinion in genetics & development · 2016Review
- Developmental origin of postnatal cardiomyogenic progenitor cells.Future science OA · 2016Article
- Oncostatin M-induced cardiomyocyte dedifferentiation regulates the progression of diabetic cardiomyopathy through B-Raf/Mek/Erk signaling pathway.Acta biochimica et biophysica Sinica · 2016Article
- Article
- Pharmacological Therapy in the Heart as an Alternative to Cellular Therapy: A Place for the Brain Natriuretic Peptide?Stem cells international · 2016Review
- Effective top-down LC/MS+ method for assessing actin isoforms as a potential cardiac disease marker.Analytical chemistry · 2015Article
- Oestrogen enhances cardiotoxicity induced by Sunitinib by regulation of drug transport and metabolism.Cardiovascular research · 2015Article
- Harnessing fetal and adult genetic reprograming for therapy of heart disease.Journal of nature and science · 2015Article
- Downregulated protein expression of transcriptional activator ELK-1 in atrial myocardium of chronic AF patients.International journal of clinical and experimental pathology · 2015Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Differentiation of foetal cardiomyocytes is accompanied by sequential actin isoform expression, i.e. down-regulation of the 'embryonic' alpha smooth muscle actin, followed by an up-regulation of alpha skeletal actin (alphaSKA) and a final predominant expression of alpha cardiac actin (alphaCA). Our objective was to detect whether re-expression of alphaSKA occurred during cardiomyocyte dedifferentiation, a phenomenon that has been observed in different pathologies characterized by myocardial dysfunction. Immunohistochemistry of alphaCA, alphaSKA and cardiotin was performed on left ventricle biopsies from human patients after coronary bypass surgery. Furthermore, actin isoform expression was investigated in left ventricle samples of rabbit hearts suffering from pressure- and volume-overload and in adult rabbit ventricular cardiomyocytes during dedifferentiation in vitro. Atrial goat samples up to 16 weeks of sustained atrial fibrillation (AF) were studied ultrastructurally and were immunostained for alphaCA and alphaSKA. Up-regulation of alphaSKA was observed in human ventricular cardiomyocytes showing down-regulation of alphaCA and cardiotin. A patchy re-expression pattern of alphaSKA was observed in rabbit left ventricular tissue subjected to pressure- and volume-overload. Dedifferentiating cardiomyocytes in vitro revealed a degradation of the contractile apparatus and local re-expression of alphaSKA. Comparable alphaSKA staining patterns were found in several areas of atrial goat tissue during 16 weeks of AF together with a progressive glycogen accumulation at the same time intervals. The expression of alphaSKA in adult dedifferentiating cardiomyocytes, in combination with PAS-positive glycogen and decreased cardiotin expression, offers an additional tool in the evaluation of myocardial dysfunction and indicates major changes in the contractile properties of these cells.
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