Atherosclerosis is universally recognized as a chronic lipid-induced inflammation of the vessel wall in response to dyslipidemia and haemodynamic stress involving dysfunction and activation of resident vascular cells as well as infiltration of leukocytes. As members of nonprotein-coding RNAs, the long noncoding RNAs (lncRNAs) are implicated in various biological processes. Accumulating evidences suggest that lncRNAs regulate the function of vascular wall, activation of macrophages, lipid metabolism and immune response. Here, we review the effects of lncRNAs on the progress of atherosclerosis.

Atherosclerosis is the leading cause of morbidity and mortality worldwide. The underlying pathogenesis involves multiple metabolic disorders, endothelial dysfunction and a maladaptive immune response, and leads to chronic arterial wall inflammation. Numerous normal physiological activities exhibit daily rhythmicity, including energy metabolism, vascular function and inflammatory immunoreactions, and disrupted or misaligned circadian rhythms may promote the progression of atherosclerosis. However, the association between the circadian rhythm and atherosclerosis remains to be fully elucidated. In the present review, the effects of the circadian rhythm on atherosclerosis progression are discussed.

Neuroinflammation mediated by activated microglia plays a pivotal role in the pathogenesis of neurological disorders, including hypoxic injury of the developing brain. Thymosin β4 (Tβ4), the major G-actin-sequestering molecule, has an anti-inflammatory effect and has been used to treat various neurological diseases. However, the effect of Tβ4 on hypoxia-induced microglia activation in the developing brain remains unclear. We investigate here the effect of Tβ4 on microglia activation of neonatal rats after hypoxia exposure. Tβ4 treatment was carried out on 1-day-old rats and BV-2 cells. Tβ4 expression in microglia was determined by quantitative real time-PCR, western blotting, and immunofluorescence staining. Secretion of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and nitric oxide (NO) was assessed by enzyme-linked immunosorbent assay and colorimetric assay. mRNA expression of TNF-α and IL-1β, and microRNA 146a expression was determined by quantitative real time-PCR. We showed that Tβ4 treatment significantly inhibited secretion of inflammatory mediators in the cerebellum of neonatal rats following hypoxia injury. Increased expression of endogenous Tβ4 in microglia was observed both in hypoxic rats and in BV-2 cells. Tβ4 treatment significantly inhibited the expression and secretion of hypoxia-induced TNF-α, IL-1β, and NO. Remarkably, microRNA 146a expression was found to have increased in Tβ4-treated BV-2 cells. We demonstrated the anti-inflammatory effect of Tβ4 in neonatal rats following hypoxic brain injury. More importantly, our data reveal, for the first time, that Tβ4 inhibits microglia activation in vitro. Therefore, this study contributes to understanding the role and mechanism of Tβ4 function in central nervous system diseases.

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The data in our study indicated that HMGB1 may promote atherosclerosis progression via modulating the imbalance in the Treg/Th17 ratio.