Geometry and length control of 3D engineered heart tissues using direct laser writing

Karakan, M. Çağatay; Ewoldt, Jourdan K.; Segarra, Addianette J.; Sundaram, Subramanian; Wang, Miranda C.; White, Alice E.; Chen, Christopher S.; Ekinci, Kamil L.

doi:10.1039/d3lc00752a

Lab Chip

2024

DOI: 10.1039/d3lc00752a

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Geometry and length control of 3D engineered heart tissues using direct laser writing

M. Çağatay Karakan,

Jourdan K. Ewoldt,

Addianette J. Segarra

et al.

Abstract: Geometry and mechanical characteristics of the surrounding environment affect the structure and function of engineered heart tissues (EHT). Here, we employed a 3D tissue culture platform fabricated using two-photon direct...

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2024

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References 44 publications

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Hypertrophic cardiomyopathy–associated mutations drive stromal activation via EGFR-mediated paracrine signaling

Ewoldt,

Wang,

McLellan

et al. 2024

Sci. Adv.

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Hypertrophic cardiomyopathy (HCM) is characterized by thickening of the left ventricular wall, diastolic dysfunction, and fibrosis, and is associated with mutations in genes encoding sarcomere proteins. While in vitro studies have used human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) to study HCM, these models have not examined the multicellular interactions involved in fibrosis. Using engineered cardiac microtissues (CMTs) composed of HCM-causing MYH7 -variant hiPSC-CMs and wild-type fibroblasts, we observed cell-cell cross-talk leading to increased collagen deposition, tissue stiffening, and decreased contractility dependent on fibroblast proliferation. hiPSC-CM conditioned media and single-nucleus RNA sequencing data suggested that fibroblast proliferation is mediated by paracrine signals from MYH7 -variant cardiomyocytes. Furthermore, inhibiting epidermal growth factor receptor tyrosine kinase with erlotinib hydrochloride attenuated stromal activation. Last, HCM-causing MYBPC3 -variant CMTs also demonstrated increased stromal activation and reduced contractility, but with distinct characteristics. Together, these findings establish a paracrine-mediated cross-talk potentially responsible for fibrotic changes observed in HCM.

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Hypertrophic cardiomyopathy–associated mutations drive stromal activation via EGFR-mediated paracrine signaling

Ewoldt,

Wang,

McLellan

et al. 2024

Sci. Adv.

View full text Add to dashboard Cite

show abstract

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Geometry and length control of 3D engineered heart tissues using direct laser writing

Abstract: Geometry and mechanical characteristics of the surrounding environment affect the structure and function of engineered heart tissues (EHT). Here, we employed a 3D tissue culture platform fabricated using two-photon direct...

Cited by 1 publication

References 44 publications

Hypertrophic cardiomyopathy–associated mutations drive stromal activation via EGFR-mediated paracrine signaling

Hypertrophic cardiomyopathy–associated mutations drive stromal activation via EGFR-mediated paracrine signaling

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