Single-nuclei multiomics analysis identifies abnormal cardiomyocytes in a murine model of cardiac development

Riley Leonard, Yi Zhao, Steven Eliason, Kathy Zimmerman, Ariana Batz, Cathy J. Hatcher, Robert M. Weiss, Mason Sweat, Xiao Li and Brad A. Amendt ()
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Riley Leonard: Department of Anatomy and Cell Biology
Yi Zhao: Texas Heart Institute
Steven Eliason: Department of Anatomy and Cell Biology
Kathy Zimmerman: Department of Internal Medicine
Ariana Batz: Department of Internal Medicine
Cathy J. Hatcher: Philadelphia College of Osteopathic Medicine
Robert M. Weiss: Department of Internal Medicine
Mason Sweat: Harvard University
Xiao Li: Texas Heart Institute
Brad A. Amendt: Department of Anatomy and Cell Biology

Nature Communications, 2025, vol. 16, issue 1, 1-21

Abstract: Abstract Transcription factors such as Tbx5, Gata4, Mef2c and Pitx2 are required during cardiac development, and in adult cardiac homeostasis. We demonstrate that the gene dosage and modulation of these factors are mediated in vivo by the miR-200 family. Inhibition of a single miR-200 family member within the cluster results in defects of the left ventricle and cardiomyocyte maturation during development. Inhibition of the entire miR-200 family results in a ventricular septal defect and embryonic lethality by embryonic day (E)16.5. Inhibition of each miR-200 family has distinct heart phenotypes in cell specific differentiation and maturation. snRNA-sequencing reveals an immature cardiomyocyte cell state, suggesting reduced differentiation of these cells. The miR-200 family members are critical regulators of early cardiac development through maintaining cardiomyocyte differentiation and maturation. In this report, we identify several transcription factors regulated by miR-200 during heart development, a role for miR-200 in specific heart defects, and an abnormal cardiomyocyte population.

Date: 2025
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DOI: 10.1038/s41467-025-62208-9

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