ArticleIntegrative biology : quantitative biosciences from nano to macro2020
Regulation of calcium dynamics and propagation velocity by tissue microstructure in engineered strands of cardiac tissue.
Article in Integrative biology : quantitative biosciences from nano to macro, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed.
- 3D bioprinting of microfluidic systems for cardiac regenerative medicine: from biofabrication to organ-on-a-chip.Journal of biological engineering · 2026Review
- Geometry and length control of 3D engineered heart tissues using direct laser writing.Lab on a chip · 2024Article
- Regulation of oxytocin-induced calcium transients and gene expression in engineered myometrial tissues by tissue architecture and matrix rigidity.Current research in physiology · 2023Article
- A myocardial infarct border-zone-on-a-chip demonstrates distinct regulation of cardiac tissue function by an oxygen gradient.Science advances · 2022Article
- Modeling Patient-Specific Muscular Dystrophy Phenotypes and Therapeutic Responses in Reprogrammed Myotubes Engineered on Micromolded Gelatin Hydrogels.Frontiers in cell and developmental biology · 2022Article
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Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Disruptions to cardiac tissue microstructure are common in diseased or injured myocardium and are known substrates for arrhythmias. However, we have a relatively coarse understanding of the relationships between myocardial tissue microstructure, propagation velocity and calcium cycling, due largely to the limitations of conventional experimental tools. To address this, we used microcontact printing to engineer strands of cardiac tissue with eight different widths, quantified several structural and functional parameters and established correlation coefficients. As strand width increased, actin alignment, nuclei density, sarcomere index and cell aspect ratio decreased with unique trends. The propagation velocity of calcium waves decreased and the rise time of calcium transients increased with increasing strand width. The decay time constant of calcium transients decreased and then slightly increased with increasing strand width. Based on correlation coefficients, actin alignment was the strongest predictor of propagation velocity and calcium transient rise time. Sarcomere index and cell aspect ratio were also strongly correlated with propagation velocity. Actin alignment, sarcomere index and cell aspect ratio were all weak predictors of the calcium transient decay time constant. We also measured the expression of several genes relevant to propagation and calcium cycling and found higher expression of the genes that encode for connexin 43 (Cx43) and a subunit of L-type calcium channels in thin strands compared to isotropic tissues. Together, these results suggest that thinner strands have higher values of propagation velocity and calcium transient rise time due to a combination of favorable tissue microstructure and enhanced expression of genes for Cx43 and L-type calcium channels. These data are important for defining how microstructural features regulate intercellular and intracellular calcium handling, which is needed to understand mechanisms of propagation in physiological situations and arrhythmogenesis in pathological situations.
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