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Docosahexaenoic acid (DHA) is reported to have the potential to ameliorate pulmonary arterial hypertension (PAH), while the specific mechanism is still obscure. This study aims to investigate the function of DHA in pulmonary artery smooth muscle cells (PASMCs) and explore the underlying mechanism. In our study, DHA was used to incubate PASMCs. Cytosolic‐free Ca2+ concentration ([Ca2+]cyt) was measured using Fluo‐3 AM method. Real‐time polymerase chain reaction was used to detect microRNA‐16 (miR‐16) and calcium‐sensing receptor (CaSR) messenger RNA expression levels. CCK‐8 assay, BrdU assay, and Transwell assay were employed to detect the effects of DHA on proliferation and migration of PASMCs. CaSR was confirmed as a direct target of miR‐16 using dual‐luciferase assay, polymerase chain reaction, and Western blot analysis. It was found that DHA significantly inhibited PASMC proliferation and migration and decreased [Ca2+]cyt. After transfection of miR‐16 mimics, proliferation and migration ability of PASMCs were significantly inhibited, whereas opposite effects were observed after miR‐16 inhibition. [Ca2+]cyt was also inhibited by miR‐16 transfection. DHA then promoted the expression of miR‐16, and the effects of DHA on PASMCs were annulled when miR‐16 was inhibited. CaSR was identified as a direct target of miR‐16. CaSR was inhibited directly by miR‐16 and indirectly by DHA. In conclusion, DHA inhibits the proliferation and migration of PASMCs, and probably ameliorates PAH via regulating miR‐16/CaSR axis. [ABSTRACT FROM AUTHOR]

Recent studies indicate that disturbed structure and function of microglia can cause depression and associated neurogenesis impairments. Our previous work has demonstrated that exogenous fibroblast growth factor 2 (FGF2) reverses the depressive-like behaviors and the impaired hippocampal neurogenesis in a neuroinflammatory model of depression. However, whether and how the antidepressant effects of FGF2 involve the modulation of microglia activation has not been elucidated. In this study, to examine the effects of FGF2 on microglia activation, exogenous FGF2 was supplemented to the lateral ventricle of rats during the neuroinflammatory state induced by central lipopolysaccharides (LPS) administrations. It was found that FGF2 infusions reversed the LPS-induced depressive-like behaviors and inhibited the hippocampal microglia activation. In LPS-treated rats, FGF2 decreased the level of pro-inflammatory cytokines including interlukin-1β (IL-1β), IL-6 and tumor necrosis factor (TNF)-α, increased the level of IL-10, the anti-inflammatory cytokine and reversed the decreased expression of CX3CL1, a chemokine mainly expressed by neurons and keeping microglia in surveillance. Further, we examined the effects of inhibited FGF2 signaling by administration of SU5402, an FGFR inhibitor. It was found that SU5402 itself evoked depressive-like behaviors, induced microglia activation, increased production of pro-inflammatory cytokines including IL-1β, IL-6 and TNF-α, and decreased the expression of CX3CL1. Two lines of results that FGF2 signaling and FGFR inhibitor can effectively but oppositely modulate the regulation of microglia and the generation of depressive-like behavior, suggesting that microglia-regulated mechanisms may underlie the antidepressant role of FGF2. The present data provide novel insights into the understanding of mechanism of neuroinflammation-associated depression and may serve as a novel mechanism-based target for the treatment of inflammation-related depression. [ABSTRACT FROM AUTHOR]

Abstract: A model for option pricing of fractional version of the Merton model with ‘Hurst exponent’ being in is established with transaction costs. In particular, for the minimal price of an option under transaction costs is obtained, which displays that the timestep and the ‘Hurst exponent’ play an important role in option pricing with transaction costs. [Copyright &y& Elsevier]

Abstract: This paper deals with the problem of discrete-time option pricing by the mixed Brownian–fractional Brownian model with transaction costs. By a mean-self-financing delta hedging argument in a discrete-time setting, a European call option pricing formula is obtained. In particular, the minimal pricing of an option under transaction costs is obtained, which shows that timestep and Hurst exponent play an important role in option pricing with transaction costs. In addition, we also show that there exists fundamental difference between the continuous-time trade and discrete-time trade and that continuous-time trade assumption will result in underestimating the value of a European call option. [Copyright &y& Elsevier]