ABSTRACT
Microparticles are small vesicles with a diameter ranging from 0.1 to 1 µm that fall off from cell membranes through germination when cells are activated or apoptotic. Microparticle contains proteins, cytokines, mRNA, microRNA and other substances, and exerts a variety of biological functions. Microparticle plays an important role in endothelial cell dysfunction, inflammation, and smooth muscle cell proliferation and migration in the development and progression of atherosclerosis. Highlevel microparticles in circulation are not only biomarkers of vascular injury in atherosclerosis patients, but also potential diagnostic and therapeutic targets of atherosclerosis. This review focuses on the role of microparticle in the development and progression of atherosclerosis, and sums up the related research progresses at the cellular level.
ABSTRACT
Aortic disease (AD) consists of a series of life-threatening diseases caused by aortic wall lesions. Up to now little has been known about the etiology of non-hereditary AD. Vascular smooth muscle cells (VSMC) are the major components of the medial aortic wall and can toggle between a contractile phenotype and a synthetic phenotype. The excessive transformation of VSMC from contractile state to synthetic state plays an important role in the development and progression of AD. Although there are many researches on the regulation of VSMS phenotype switch, how these regulatory pathways operate harmoniously and the what relationship between them remain to be elucidated. Here in this paper we reviewed the existing regulatory mechanisms of VSMC phenotype switch.
ABSTRACT
Objective: To investigate the influence of sufentanil on calcium-activated K+ channels (IKCa) in rat abdominal aortic smooth muscle cells, and to investigate its role in dilation of blood vessels. Methods: Rat abdominal aortic smooth muscle cells (AASMCs) were freshly obtained by enzymatic digestion. Whole-cell voltage-clamp technique was used to assess the effect of sufentanil (1 × 10-8, 3 × 10-8, 1 × 10-7 mol/L) on IKCa. Results: Sufentanil significantly increased the amplitude of IKc compared with the control group (P < 0.05 or P < 0.01). The effect of sufentanil was reversible and in a concentration-dependent manner. Conclusion: Sufentanil can promote the activation of KCa channel in rat AASMCs, which might be related to the vasodilatory effect of sufentanil observed in clinical practice.
ABSTRACT
Objective: To investigate the changes of histone deacetylase (HDAC) activity during chronic asthma and its effects on the phenotype and biological activities of airway smooth muscle cells. Methods: Chronic asthma model was established with mice using repeated sensitization and challenge with OVA, and the lung was homogenated for total HDAC activity assay. Rat airway smooth muscle cells and human bronchial smooth muscle cells were stimulated with trichostatin A (TSA), an HDAC inhibitor. The effect of HDAC inhibition on phenotype switching was detected by Western Blotting analysis, and its effects on proliferation, migration and contraction of smooth muscle cells were examined by MTT, Transwell and gel contraction, respectively. Results: The total HDAC activity was significantly decreased in chronic asthmatic mice compared with saline-treated controls ([0.371±0.054] vs [0.603±0.034] μmol/(L·μg), P<0.01). Incubation of the rat trachea ring and human bronchial smooth muscle cells with TSA (0.5 μmol/L) for 12-24 h increased the expression of α-sm-actin and SM22-α. TSA significantly decreased cell number after 24 h treatment ([1.719±0.044)×10 4 vs ([1.911±0.048]×104, P<0.05) and 48 h [1.808±0.009]×104 vs [2.537±0.01]×10 4, P<0.05) compared with DMSO controls. TSA treatment for 24 h also significantly decreased the migrated cells compared with the PDGF-treated cells (52±7.5 vs 88±7.632, P<0.05). Furthermore, the gel contraction rate was significantly lower in the TSA-treated cells than in the DMSO or PDGF-treated cells ([9.885±7.084]% vs [44.844±3.808]% and [41.315±7.943]%, P<0.05). Conclusion: HDAC activity is decreased in the lung of chronic asthmatic mice, which may be related to switching of the airway smooth muscle cells to a "contractic" phenotype, but with no increase of their contraction capability.