Adaptation of glycocalyx, nitric oxide synthase expression and vascular cell apoptosis in conduit arteries of tail-suspended rats.
Hongyan KangChenglin WuYuxin QuMenghan GaoWeichen ZhangAnqiang SunXiaoyan DengPublished in: Clinical and experimental pharmacology & physiology (2019)
The importance of vascular cell glycocalyx in mechanotransduction has been demonstrated by many studies. The simulated microgravity induced a region-dependent adaptation of arterial glycocalyx including its thickness, coverage, and gene expression in conduit arteries of tail-suspended rats has been reported in our previous studies. Herein, we extended this line of research by quantifying the mRNA levels of three nitric oxide synthase (NOSI, NOSII, and NOSIII) and evaluating the apoptotic rates of endothelial cells (ECs) and smooth muscle cells (SMCs) in the common carotid artery, abdominal aorta, and femoral artery of 3 week tail-suspended rats. Results indicated that the tail suspension of rats induced about 0.36, 0.22, and 0.33 fold down-regulation of NOSI, NOSII, and NOSIII in the abdominal aorta, while 3.21, and 3.48 fold up-regulation of NOSII and NOSIII in the carotid artery and no significant effects on three NOS isoforms in the femoral artery. Moreover, the apoptosis of ECs and SMCs were significantly inhibited in both carotid artery and abdominal aorta, while enhanced in the femoral artery of the tail-suspended rats. A linear positive correlation exists between the normalized coverage of the glycocalyx and the normalized NOSI and NOSIII mRNA levels. These results indicated that the redistribution of haemodynamics in the conduit arteries of 3 week tail-suspended rats regulated the glycocalyx, NOS expression, and vascular cell apoptosis in a region-dependent manner, contributing to the final vascular remodelling under simulated microgravity condition.
Keyphrases
- nitric oxide synthase
- nitric oxide
- gene expression
- endothelial cells
- cell death
- aortic valve
- oxidative stress
- pulmonary artery
- randomized controlled trial
- cell proliferation
- binding protein
- stem cells
- healthcare
- dna methylation
- coronary artery
- pulmonary arterial hypertension
- endoplasmic reticulum stress
- diabetic rats
- signaling pathway
- mesenchymal stem cells
- anti inflammatory
- single cell
- bone marrow
- affordable care act
- stress induced
- cell cycle arrest
- study protocol