Tenascin C+ myofibroblasts exacerbate vascular neointimal hyperplasia by propagation of nerve-macrophage interactions

Neointimal hyperplasia (NIH) is a major pathological feature of vascular injury, yet the underlying cellular and molecular drivers remain poorly understood. Here, we combine lineage tracing, single-cell transcriptomics, genetic mouse models and live imaging to identify a population of Tenascin C-expressing (Tnc+) myofibroblasts (MFs) that emerges in both a ligation-induced mouse model of carotid artery NIH and clinical NIH specimens. Overall design: Carotid arteries from Tnc-cKO mice were harvested two weeks post vascular ligation. Arteries were enzymatically digested to single-cell suspension, and then scRNA-seq libraries were built with the 10x Genomics platform.