ArticleProceedings of the National Academy of Sciences of the United States of America1997
Slow skeletal troponin I gene transfer, expression, and myofilament incorporation enhances adult cardiac myocyte contractile function.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 117 citations in OpenAlex.
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- Cardiac Sarcomere Signaling in Health and Disease.International journal of molecular sciences · 2022Review
- Human iPSC-engineered cardiac tissue platform faithfully models important cardiac physiology.American journal of physiology. Heart and circulatory physiology · 2021Article
- Troponin Variants as Markers of Skeletal Muscle Health and Diseases.Frontiers in physiology · 2021Review
- Sarcomere integrated biosensor detects myofilament-activating ligands in real time during twitch contractions in live cardiac muscle.Journal of molecular and cellular cardiology · 2020Article
- Electrospun Scaffolds and Induced Pluripotent Stem Cell-Derived Cardiomyocytes for Cardiac Tissue Engineering Applications.Bioengineering (Basel, Switzerland) · 2020Review
- Cardiomyocyte maturation: advances in knowledge and implications for regenerative medicine.Nature reviews. Cardiology · 2020Review
- Increased myocyte calcium sensitivity in end-stage pediatric dilated cardiomyopathy.American journal of physiology. Heart and circulatory physiology · 2019Article
- Learn from Your Elders: Developmental Biology Lessons to Guide Maturation of Stem Cell-Derived Cardiomyocytes.Pediatric cardiology · 2019Review
- TnI Structural Interface with the N-Terminal Lobe of TnC as a Determinant of Cardiac Contractility.Biophysical journal · 2018Article
- Hypertrophic Cardiomyopathy Cardiac Troponin C Mutations Differentially Affect Slow Skeletal and Cardiac Muscle Regulation.Frontiers in physiology · 2017Article
- Molecular inotropy mediated by cardiac miR-based PDE4D/PRKAR1α/phosphoprotein signaling.Scientific reports · 2016Article
- TNNI1, TNNI2 and TNNI3: Evolution, regulation, and protein structure-function relationships.Gene · 2016Review
- DNA methylation regulates mouse cardiac myofibril gene expression during heart development.Journal of biomedical science · 2015Article
- Gene transfer into cardiac myocytes.Methods in molecular biology (Clifton, N.J.) · 2015Article
- Acquisition of a quantitative, stoichiometrically conserved ratiometric marker of maturation status in stem cell-derived cardiac myocytes.Stem cell reports · 2014Article
- Cell biology of sarcomeric protein engineering: disease modeling and therapeutic potential.Anatomical record (Hoboken, N.J. : 2007) · 2014Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The functional significance of the developmental transition from slow skeletal troponin I (ssTnI) to cardiac TnI (cTnI) isoform expression in cardiac myocytes remains unclear. We show here the effects of adenovirus-mediated ssTnI gene transfer on myofilament structure and function in adult cardiac myocytes in primary culture. Gene transfer resulted in the rapid, uniform, and nearly complete replacement of endogenous cTnI with the ssTnI isoform with no detected changes in sarcomeric ultrastructure, or in the isoforms and stoichiometry of other myofilament proteins compared with control myocytes over 7 days in primary culture. In functional studies on permeabilized single cardiac myocytes, the threshold for Ca2+-activated contraction was significantly lowered in adult cardiac myocytes expressing ssTnI relative to control values. The tension-Ca2+ relationship was unchanged from controls in primary cultures of cardiac myocytes treated with adenovirus containing the adult cardiac troponin T (TnT) or cTnI cDNAs. These results indicate that changes in Ca2+ activation of tension in ssTnI-expressing cardiac myocytes were isoform-specific, and not due to nonspecific functional changes resulting from overexpression of a myofilament protein. Further, Ca2+-activated tension development was enhanced in cardiac myocytes expressing ssTnI compared with control values under conditions mimicking the acidosis found during myocardial ischemia. These results show that ssTnI enhances contractile sensitivity to Ca2+ activation under physiological and acidic pH conditions in adult rat cardiac myocytes, and demonstrate the utility of adenovirus vectors for rapid and efficient genetic modification of the cardiac myofilament for structure/function studies in cardiac myocytes.
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