Indole-3-acetic acid enhances the co-transport of proton and phenanthrene mediated by TaSAUR80-5A in wheat roots.

Polycyclic aromatic hydrocarbons (PAHs) are a type of organic pollution that can accumulate in crops and hazard human health. This study used phenanthrene (PHE) as a model PAH and employed hydroponic experiments to illustrate the role of indole-3-acetic acid (IAA) in the regulation of PHE accumulation in wheat roots. At optimal concentrations, wheat roots treated with PHE + IAA showed a 46.9% increase in PHE concentration, whereas treatment with PHE + P-chlorophenoxyisobutyric acid resulted in a 38.77% reduction. Transcriptome analysis identified TaSAUR80-5A as the crucial gene for IAA-enhancing PHE uptake. IAA increases plasma membrane H+-ATPase activity, promoting active transport of PHE via the PHE/H+ cotransport mechanism. These results provide not only the theoretical basis necessary to better understand the function of IAA in PAHs uptake and transport by staple crops, but also a strategy for controlling PAHs accumulation in staple crops and enhancing phytoremediation of PAH-contaminated environments.

Decreased Netrin-1 and Correlated Th17/Tregs Balance Disorder in Aß1-42 Induced Alzheimer's Disease Model Rats.

There is increasing evidence indicating that inflammation represents a key pathological component of Alzheimer's disease (AD). A possible factor that may contribute to this process is netrin-1, a neuronal guidance molecule. This molecule has been shown to exert an unexpected immunomodulatory function. However, the potential changes and correlations of netrin-1 with T helper 17/regulatory T cells (Th17/Tregs) as related to inflammation in AD has yet to be examined. In this study, netrin-1 and Th17/Tregs balance were investigated, and the relationship among netrin-1, Th17/Tregs and cognitive function were analyzed in a rat model of AD. In this model, a bilateral intracerebroventricular administration of Amyloid ß1-42 (Aß1-42) was used to produce spatial learning and memory deficits, as well as increased neuronal apoptosis, which were detected 7 days after injection for AD7d group and 14 days for AD14d group. Netrin-1 concentrations were significantly down regulated in both serum and cerebrospinal fluid (CSF) of these AD rats, effects which were strongly correlated with cognitive deficits. Increased levels of interleukin (IL)-17 and deceased IL-10 were observed in both the circulation and CSF and were also correlated with the percent of time spent in the target quadrant of AD in these rats. These changes resulted in netrin-1 concentrations being negatively correlated with IL-17 but positively correlated with IL-10 concentrations in the serum and CSF. We also found that the Th17/Tregs balance was disrupted in these AD rats. Collectively, these findings reveal that the reduction in netrin-1 and the correlated disruption of Th17/Tregs balance in AD rats may diminish the immunosuppressive effect of netrin-1 on Th17/Tregs in AD pathogenesis.

MiR-298 Exacerbates Ischemia/Reperfusion Injury Following Ischemic Stroke by Targeting Act1.

BACKGROUND/AIMS: This study investigated the role of the microRNA miR-298 and its target Act1 in ischemic stroke. METHODS: Cell viability was assessed with the 3-(4,5-dimethythiazol-2- yl)-2,5-diphenyl tetrazolium bromide assay. Apoptotic cells were detected by flow cytometry, and mRNA and protein expression were assessed by quantitative real-time PCR and western blotting, respectively. The regulatory relationship between miR-298 and Act1 was evaluated with the luciferase assay. To clarify the role of Act1 following ischemic stroke, the transcript was knocked down by short interfering RNA. The in vitro findings were validated in a mouse model of middle cerebral artery occlusion by administration of miR-298 mimic. RESULTS: Act1 was upregulated whereas miR-298 was downregulated in ischemic stroke. miR-298 overexpression by transfection of a mimic suppressed Act1 protein levels in vitro and in vivo, and the luciferase assay showed that miR-298 directly binds to the 3' untranslated region of the Act1 transcript. miR-298 overexpression enhanced cell apoptosis and autophagy and exacerbated ischemic infarction and neurological deficits, effects that were exerted via negative regulation of Act1/c-Jun N-terminal kinase (JNK)/nuclear factor (NF)-κB signaling and downstream autophagy pathways. CONCLUSIONS: Upregulation of miR-298 following ischemic stroke promotes brain injury in vitro and vivo by inhibiting the Act1/JNK/NF-κB signaling cascade and the downstream autophagy pathway. Therapeutic strategies that target miR-298 could be beneficial for the treatment of ischemic stroke.