Myeloid Ecotropic Viral Integration Site 1 Promotes Vascular Smooth Muscle Differentiation through Activation of Myocardin
- 1Louisiana State University Health Shreveport
Abstract
Myocardin (MYOCD) is the principal trigger-switch for vascular smooth muscle cell (VSMC) growth arrest and the cyto-contractile program of differentiation. While much is known about MYOCD-dependent VSMC differentiation, limited information exists as to its transcriptional regulation. Here, we report moderate mRNA expression of Myeloid Ecotropic viral Integration Site 1 (MEIS1) in both human and mouse VSMCs. MEIS1 mRNA is reduced in parallel with myocardin mRNA and protein under conditions of VSMC de-differentiation. Loss- and gain-of-Meis1 expression studies in cultured human VSMCs and the mouse carotid artery support MEIS1 as an activator of myocardin and VSMC differentiation. CRISPR-mediated knockout of the endogenous Meis1 gene in vitro and elicited lower levels of VSMC contractile markers and an increase in growth rate. Similarly, Femoral artery wire injury, in mice lacking Meis1 showed and increased of neointima formation. Mechanistically, we identified a conserved MEIS1 response element in the proximal promoter of myocardin, that appears to contribute to the promoter activity, suggesting a potential regulatory interaction. These results suggest a previously unrecognized role for the homeodomain protein MEIS1 in the activation of myocardin and the quiescent, VSMC differentiated state.
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BibTeX
@misc{wally2026myeloid,
title = {{Myeloid Ecotropic Viral Integration Site 1 Promotes Vascular Smooth Muscle Differentiation through Activation of Myocardin}},
author = {A. Wally and S. Joshi and J. Doja and A. Kumar and O. J. Slivano and S. H. Griffin and K. Dong and L. Maticc and U. Hedin and X. Long and A. R. Salem},
howpublished = {bioRxiv},
year = {2026},
month = sep,
doi = {10.64898/2026.09.26.751066},
url = {https://www.biorxiv.org/content/10.64898/2026.09.26.751066v1},
note = {CC BY},
}
RIS
TY - UNPB
TI - Myeloid Ecotropic Viral Integration Site 1 Promotes Vascular Smooth Muscle Differentiation through Activation of Myocardin
AU - A. Wally
AU - S. Joshi
AU - J. Doja
AU - A. Kumar
AU - O. J. Slivano
AU - S. H. Griffin
AU - K. Dong
AU - L. Maticc
AU - U. Hedin
AU - X. Long
AU - A. R. Salem
PY - 2026
DA - 2026/09/26
PB - bioRxiv
DO - 10.64898/2026.09.26.751066
UR - https://www.biorxiv.org/content/10.64898/2026.09.26.751066v1
AB - Myocardin (MYOCD) is the principal trigger-switch for vascular smooth muscle cell (VSMC) growth arrest and the cyto-contractile program of differentiation. While much is known about MYOCD-dependent VSMC differentiation, limited information exists as to its transcriptional regulation. Here, we report moderate mRNA expression of Myeloid Ecotropic viral Integration Site 1 (MEIS1) in both human and mouse VSMCs. MEIS1 mRNA is reduced in parallel with myocardin mRNA and protein under conditions of VSMC de-differentiation. Loss- and gain-of-Meis1 expression studies in cultured human VSMCs and the mouse carotid artery support MEIS1 as an activator of myocardin and VSMC differentiation. CRISPR-mediated knockout of the endogenous Meis1 gene in vitro and elicited lower levels of VSMC contractile markers and an increase in growth rate. Similarly, Femoral artery wire injury, in mice lacking Meis1 showed and increased of neointima formation. Mechanistically, we identified a conserved MEIS1 response element in the proximal promoter of myocardin, that appears to contribute to the promoter activity, suggesting a potential regulatory interaction. These results suggest a previously unrecognized role for the homeodomain protein MEIS1 in the activation of myocardin and the quiescent, VSMC differentiated state.
ER -