Abstract
In the previous report, Meox1 was found to promote SMCs phenotypic modulation and injury-induced vascular remodeling by regulating the FAK-ERK1/2-autophagy signaling cascade (Wu et al., 2017) [1]. Here, we presented new original data on the involvement of Mesoderm/mesenchyme homeobox gene l (Meox1) in balloon-injury-induced neointima formation of rat. In rat carotid artery balloon injury model to induce vascular remodeling, Meox1 was induced in vascular smooth muscle cell (SMCs) of rat carotid arteries. Most proliferating cell nuclear antigen (PCNA)-positive cells also expressed Meox1. These data suggested that Meox1 may be involved in SMCs proliferation during injury-induced neointima formation. Furthermore, knocked down its expression in injured arteries by adenoviral delivery of Meox1 short hairpin RNA (shRNA) (shMeox1), neointima formation was significantly inhibited. Elastin staining also confirmed the reduction of neointima in Meox1 shRNA-transduced arteries. Moreover, knockdown of Meox1 decreased the collagen production/deposition that was significantly increased in neointima induced by balloon injury.
Highlights
In the previous report, Meox1 was found to promote SMCs phenotypic modulation and injury-induced vascular remodeling by regulating the FAK-ERK1/2-autophagy signaling cascade (Wu et al, 2017) [1]
In rat carotid artery balloon injury model to induce vascular remodeling, Meox1 was induced in vascular smooth muscle cell (SMCs) of rat carotid arteries
Most proliferating cell nuclear antigen (PCNA)-positive cells expressed Meox1. These data suggested that Meox1 may be involved in SMCs proliferation during injury-induced neointima formation
Summary
Figures and text The images were obtained from Microscope, Nikon 80i. Immunoblotting were measured with densitometry by Image J software (NIH). To determine the role of Meox in SMCs phenotypic modulation in vivo, we used rat carotid artery balloon injury model to induce vascular remodeling. Injury induced progressive neointima formation in the arteries (Fig. 1A). To determine if Meox was expressed in SMCs and if Meox1-expressing cells contributed to the SMCs proliferation, we co-stained Meox with smooth muscle α-actin (α-SMA) and PCNA in arteries injured for 14 days, respectively. To determine if Meox plays a role in the injury-induced neointimal formation, we knocked down its expression in injured arteries by adenoviral delivery of Meox shRNA. Knockdown of Meox decreased the collagen production/deposition that was significantly increased in neointima by balloon injury (Fig. 2E), which is likely due to the role of Meox in modulating SMCs phenotype in the neointima
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