Docosahexaenoic acid inhibits Ca influx and downregulates CaSR by upregulating microRNA-16 in pulmonary artery smooth muscle cells.

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.

MicroRNA-143-5p modulates pulmonary artery smooth muscle cells functions in hypoxic pulmonary hypertension through targeting HIF-1α.

This paper explores the potential mechanism of microRNA-143-5p regulation effects on pulmonary artery smooth muscle cells (PASMCs) functions in hypoxic pulmonary hypertension (HPH) via targeting HIF-1a, which may offer a new idea for HPH therapy. PASMCs were transfected with mimics control/miR-143-5p mimics or inhibitor control/miR-143-5p inhibitor. We used Western blotting and RT-qPCR to detect the protein and mRNA expressions, CCK-8 assay to detect cellular viability, Annexin V-FITC/PI staining and caspase- 3/cleaved caspase-3 protein to evaluate cellular apoptosis, transwell migration experiment for cellular migration measurement and Dual luciferase reporter gene assay to prove the target of miR-143-5p.

Fibroblast Growth Factor 2 Modulates Hippocampal Microglia Activation in a Neuroinflammation Induced Model of Depression.

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.

Blocking p38 Signaling Reduces the Activation of Pro-inflammatory Cytokines and the Phosphorylation of p38 in the Habenula and Reverses Depressive-Like Behaviors Induced by Neuroinflammation.

Increasing evidence has demonstrated that neuroinflammation contributes to the development of depressive-like behaviors, in both animal models and human patients; however, the brain areas and signaling pathways involved are still elusive. Recent studies have suggested novel roles of the habenula in the onset of depression and other psychiatric disorders; however, there is no evidence for whether the habenula has a function in neuroinflammation-induced depression. Using an animal model of depression, which is induced by the repeated central administration of lipopolysaccharide (LPS), we examined whether cytokine expression and p38 signal activation in the habenula were involved in the depressive-like behaviors.

Temporal Differentiation of Crop Growth as One of the Drivers of Intercropping Yield Advantage.

Intercropping studies usually focus on yield advantage and interspecific interactions but few quantify temporal niche differentiation and its relationship with intercropping yield advantage. A field experiment conducted in northwest China in 2013 and 2014 examined four intercropping systems (oilseed rape/maize, oilseed rape/soybean, potato/maize, and soybean/potato) and the corresponding monocultures. Total dry matter data collected every 20 d after maize emergence were fitted to logistic models to investigate the temporal dynamics of crop growth and interspecific interactions.

Exogenous FGF2 reverses depressive-like behaviors and restores the suppressed FGF2-ERK1/2 signaling and the impaired hippocampal neurogenesis induced by neuroinflammation.

Our previous work demonstrated that neuroinflammation evoked by triple repeated central LPS challenges inhibited adult hippocampal neurogenesis that were correlated with the depressive-like behavioral symptoms induced by neuroinflammation. These findings suggest that hippocampal neurogenesis might be one of biological mechanisms underlying depression induced by neuroinflammation and targeting neurogenesis might lead to new therapeutic strategies for the treatment of depression. In this study, we manipulated adult hippocampal neurogenesis using fibroblast growth factor 2 (FGF2), one crucial molecule modulating cell proliferation and survival in central nervous system, and investigate the involvement and the potential therapeutic effects of FGF2 on neuroinflammation-induced depression.

LTBP2 is a prognostic marker in head and neck squamous cell carcinoma.

Latent transforming growth factor (TGF)-beta binding protein 2 (LTBP2) belongs to the fibrillin/LTBP extracellular matrix glycoprotein superfamily. It plays vital roles in tumorigenesis through regulating TGFβ activity, elastogenesis and maintenance of the extracellular matrix (ECM) structure. In this study, we determined the expression levels of LTBP2 mRNA and protein in head and neck squamous cell carcinoma (HNSCC) tissues and adjacent normal tissues by quantitative reverse transcription PCR (qRT-PCR) and tissue microarray immunohistochemistry analysis (TMA-IHC) respectively.

Hippocampal neurogenesis dysfunction linked to depressive-like behaviors in a neuroinflammation induced model of depression.

Our previous work found that triple central lipopolysaccharide (LPS) administration could induce depressive-like behaviors and increased central pro-inflammatory cytokines mRNA, hippocampal cytokine mRNA in particular. Since several neuroinflammation-associated conditions have been reported to impair neurogenesis, in this study, we further investigated whether the neuroinflammation induced depression would be associated with hippocampal neurogenesis dysfunction. An animal model of depression induced by triple central lipopolysaccharide (LPS) administration was used.

Comparison of stress-induced and LPS-induced depressive-like behaviors and the alterations of central proinflammatory cytokines mRNA in rats.

Although proinflammatory cytokine changes in depression have been studied widely, few investigations have searched for specific and common changes in cytokines. In the present study, two animal models of depression were compared: a chronic stress model using forced swim stress and an immune activation model using repeated central lipopolysaccharide (LPS) infusion. The levels of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6 mRNA were examined in the brain regions of the prefrontal cortex, amygdala, and hippocampus using real-time polymerase chain reaction (RT-PCR).