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The new Myh11-CreERT2-RAD mouse line is equivalent to the original line for smooth muscle cell lineage tracing but provides the critical advantage of allowing experiments in both male and female mice.
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Smooth muscle cells (SMCs) form the muscular layer of blood vessels and of the viscera in the gastrointestinal, urinary, and reproductive systems and airways.These quiescent differentiated myocytes retain a remarkable plasticity that allows for vascular remodeling and repair.In response to injury, inflammation, or hypercholesterolemia, vascular SMCs can dedifferentiate and proliferate as a protective response, but when unchecked, can drive intimal hyperplasia, atherosclerosis, and other pathologies 1, 2 .Because dedifferentiated SMCs profoundly downregulate expression of their hallmark SMC-specific contractile proteins, the roles of SMCs in cardiovascular disease were underestimated until the advent of lineage tracing approaches.Permanent genetic marking of mature SMCs using the Cre-loxP system revealed that differentiated SMCs can give rise to a broad spectrum of phenotypes including cells resembling macrophages, fibroblasts, adipocytes 3 , osteochondrocytes 4 , and stem cells 5 .These observations have led to fundamental advances in SMC biology.Paradigm-shifting revelations included confirmation that SMCs clonally expand to form lesions in atherosclerosis and intimal hyperplasia [6][7][8] and the discovery that up to ~60% of macrophage-like cells in atherosclerotic plaques are SMC-derived 9 .
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O'Brien et al. (2023) conducted an editorial in Cardiovascular disease (Smooth muscle cell biology). Myh11-CreERT2-RAD mouse line vs. Original Myh11-CreERT2 mouse line was evaluated. The new Myh11-CreERT2-RAD mouse line is equivalent to the original line for smooth muscle cell lineage tracing but provides the critical advantage of allowing experiments in both male and female mice.
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