Regional specific modulation of the glycocalyx and smooth muscle cell contractile apparatus in conduit arteries of tail-suspended rats

TLDR: The results suggest the regional-dependent adaptation of the glycocalyx in simulated microgravity condition, which may affect its mechanotransduction of shear stress to regulate the contractility of the smooth muscle, finally contributing to postspaceflight orthostatic intolerance.

Abstract: The glycocalyx is a key mechanosensor on the surfaces of vascular cells (endothelial cells and smooth muscle cells), and recently, we reported that the redistribution of the hemodynamic factors in tail-suspended (TS) hindlimb-unloaded rats induces the dimensional adaptation of the endothelial glycocalyx in a regional-dependent manner. In the present study, we investigated the coverage and gene expression of the glycocalyx and its possible relationship with smooth muscle contractility in the conduit arteries from the TS rats. The coverage of the glycocalyx, determined by the area analysis of the fluorescein isothiocyanate-labeled wheat germ agglutinin (WGA-FITC) staining to the cryosections of rat vessels, showed a 27.2% increase in the common carotid artery, a 13.3 and 8.0% decrease in the corresponding abdominal aorta and the femoral artery after 3 wk of tail suspension. The relative mRNA levels of syndecan-2, 3, 4, glypican-1, smooth muscle protein 22 (SM22), smoothelin (SMTN), and calponin were enhanced to 1.40, 1.53, 1.70, 1.90, 2.93, 2.30, and 5.23-fold, respectively, in the common carotid artery of the TS rat. However, both glycocalyx-related genes and smooth muscle contractile apparatus were totally or partially downregulated in the abdominal aorta and femoral artery of the TS rat. A linear positive correlation between the normalized coverage of glycocalyx and normalized mRNA levels of SM22, SMTN, and calponin exists. These results suggest the regional-dependent adaptation of the glycocalyx in simulated microgravity condition, which may affect its mechanotransduction of shear stress to regulate the contractility of the smooth muscle, finally contributing to postspaceflight orthostatic intolerance.