ArticleSurgery2016
Preexisting smooth muscle cells contribute to neointimal cell repopulation at an incidence varying widely among individual lesions.
Article in Surgery, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 20 citations in OpenAlex.
- Delineation of a thrombin receptor-stimulated vascular smooth muscle cell transition generating cells in the plaque-stabilizing fibrous cap.Cardiovascular research · 2025Article
- Article
- The Expanding Role of Alternative Splicing in Vascular Smooth Muscle Cell Plasticity.International journal of molecular sciences · 2021Review
- RUNX2 promotes vascular injury repair by activating miR-23a and inhibiting TGFBR2.Annals of translational medicine · 2021Article
- Celastrol ameliorates vascular neointimal hyperplasia through Wnt5a-involved autophagy.International journal of biological sciences · 2021Article
- Pathophysiological Mechanisms and Potential Therapeutic Targets in Cerebral Autosomal Dominant Arteriopathy With Subcortical Infarcts and Leukoencephalopathy (CADASIL).Frontiers in pharmacology · 2020Review
- Redistribution of Mature Smooth Muscle Markers in Brain Arteries in Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy.Translational stroke research · 2018Article
- Distinct Cellular Mechanisms Underlie Smooth Muscle Turnover in Vascular Development and Repair.Circulation research · 2018Article
- Adult Stem Cells in Vascular Remodeling.Theranostics · 2018Review
- Differential Effects of sEH Inhibitors on the Proliferation and Migration of Vascular Smooth Muscle Cells.International journal of molecular sciences · 2017Article
- An X-linked Myh11-CreERGenesis (New York, N.Y. : 2000) · 2017Article
- Notch Signaling in Endothelial Cells: Is It the Therapeutic Target for Vascular Neointimal Hyperplasia?International journal of molecular sciences · 2017Review
- Extensive Proliferation of a Subset of Differentiated, yet Plastic, Medial Vascular Smooth Muscle Cells Contributes to Neointimal Formation in Mouse Injury and Atherosclerosis Models.Circulation research · 2016Article
- Smooth muscle cell-specific Tgfbr1 deficiency attenuates neointimal hyperplasia but promotes an undesired vascular phenotype for injured arteries.Physiological reports · 2016Article
- DNA Methylation Signature of Post-injury Neointimal Cells During Vascular Remodeling in the Rat Balloon Injury Model.Molecular biology (Los Angeles, Calif.) · 2016Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundWith the diverse origin of neointimal cells, previous studies have documented differences of neointimal cell lineage composition across models, but the animal-to-animal difference has not attracted much attention, although the cellular heterogeneity may impact neointimal growth and its response to therapeutic interventions.
methodsR26R(+);Myh11-CreER(+), and R26R(+);Scl-CreER(+) mice were used to attach LacZ tags to the preexisting smooth muscle cells (SMCs) and endothelial cells (ECs), respectively. Neointimal lesions were created via complete ligation of the common carotid artery (CCA) and transluminal injury to the femoral artery (FA).
resultsLacZ-tagged SMCs were physically relocated from media to neointima and changed to a dedifferentiated phenotype in both CCA and FA lesions. The content of SMCs in the neointimal tissue, however, varied widely among specimens, ranging from 5 to 70% and 0 to 85%, with an average at low levels of 27% and 29% in CCA (n = 15) and FA (n = 15) lesions, respectively. Bone marrow cells, although able to home to the injured arteries, did not differentiate fully into SMCs after either type of injury. Preexisting ECs were located in the subendothelial region and produced mesenchymal marker α-actin, indicating endothelial-mesenchymal transition (EndoMT); however, EC-derived cells represented only 7% and 3% of the total neointimal cell pool of CCA (n = 7) and FA (n = 7) lesions, respectively. ECs located on the luminal surface exhibited little evidence of EndoMT.
conclusionNeointimal hyperplasia proceeds with a wide range of variation in its cellular composition between individual lesions. Relative to ECs, SMCs are major contributors to the lesion-to-lesion heterogeneity in neointimal cell lineage composition.
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