BAG5 Interacts with DJ-1 and Inhibits the Neuroprotective Effects of DJ-1 to Combat Mitochondrial Oxidative Damage

Loss-of-function mutations in gene encoding DJ-1 contribute to the pathogenesis of autosomal recessive early-onset familial forms of Parkinson’s disease (PD). DJ-1 is a multifunctional protein and plays a protective role against oxidative stress-induced mitochondrial damage and cell death, but the exact mechanism underlying this is not yet clearly understood. Here, using coimmunoprecipitation (Co-IP) and immunofluorescence methods, we prove that Bcl-2-associated athanogene 5 (BAG5), a BAG family member, interacts with DJ-1 in mammalian cells. Moreover, we show that BAG5 could decrease stability of DJ-1 and weaken its role in mitochondrial protection probably by influencing dimerization in stress condition. Our study reveals the relationship of BAG5 and DJ-1 suggesting a potential role for BAG5 in the pathogenesis of PD through its functional interactions with DJ-1

Paralogues from the expanded Tlr11 gene family in mudskipper (Boleophthalmus pectinirostris) are under positive selection and respond differently to LPS/Poly(I:C) challenge

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Fish-T1K (Transcriptomes of 1,000 Fishes) Project: Large-Scale Transcriptome Data for Fish Evolution Studies

Ray-finned fishes (Actinopterygii) represent more than 50 % of extant vertebrates and are of great evolutionary, ecologic and economic significance, but they are relatively underrepresented in ‘omics studies. Increased availability of transcriptome data for these species will allow researchers to better understand changes in gene expression, and to carry out functional analyses. An international project known as the “Transcriptomes of 1,000 Fishes” (Fish-T1K) project has been established to generate RNA-seq transcriptome sequences for 1,000 diverse species of ray-finned fishes. The first phase of this project has produced transcriptomes from more than 180 ray-finned fishes, representing 142 species and covering 51 orders and 109 families. Here we provide an overview of the goals of this project and the work done so far

Hypoxia Exacerbates Inflammatory Acute Lung Injury via the Toll-Like Receptor 4 Signaling Pathway

Acute lung injury (ALI) is characterized by non-cardiogenic diffuse alveolar damage and often leads to a lethal consequence, particularly when hypoxia coexists. The treatment of ALI remains a challenge: pulmonary inflammation and hypoxia both contribute to its onset and progression and no effective prevention approach is available. Here, we aimed to investigate the underlying mechanism of hypoxia interaction with inflammation in ALI and to evaluate hypoxia-inducible factor 1 alpha (HIF-1α)—the crucial modulator in hypoxia—as a potential therapeutic target against ALI. First, we developed a novel ALI rat model induced by a combined low-dose of lipopolysaccharides (LPS) with acute hypoxia. Second, we used gene microarray analysis to evaluate the inflammatory profiles of bronchi alveolar lavage fluid cells of ALI rats. Third, we employed an alveolar macrophage cell line, NR8383 as an in vitro system together with a toll-like receptor 4 (TLR4) antagonist TAK-242, to verify our in vivo findings from ALI animals. Finally, we tested the therapeutic effects of HIF-1α augmentation against inflammation and hypoxia in ALI. We demonstrated that (i) LPS upregulated inflammatory genes, tumor necrosis factor alpha (TNF-α), interleukin-1 beta (IL-1β), and interleukin-6 (IL-6), in the alveolar macrophages of ALI rats, which were further enhanced when ALI combined with hypoxia; (ii) hypoxia exposure could further enhance the upregulation of alveolar macrophageal TLR4 that was noticed in LPS-induced inflammatory ALI, conversely, TLR4 antagonist TAK-242 could suppress the macrophageal expression of TLR4 and inflammatory cytokines, including TNF-α, IL-1β, and IL-6, suggesting that the TLR4 signaling pathway as a central link between inflammation and hypoxia in ALI; (iii) manipulation of HIF-1α in vitro could suppress TLR4 expression induced by combined LPS and hypoxia, via suppressing promoter activity of the TLR4 gene; (iv) preconditioning augmentation of HIF-1α in vivo by HIF hydroxylase inhibitor, DMOG excreted protection against inflammatory, and hypoxic processes in ALI. Together, we see that hypoxia can exacerbate inflammation in ALI via the activation of the TLR4 signaling pathway in alveolar macrophages and predispose impairment of the alveolar-capillary barrier in the development of ALI. Targeting HIF-1α can suppress TLR4 expression and macrophageal inflammation, suggesting the potential therapeutic and preventative value of HIF-1α/TLR4 crosstalk pathway in ALI

Comprehensive phylogeny of ray-finned fishes (Actinopterygii) based on transcriptomic and genomic data

Our understanding of phylogenetic relationships among bony fishes has been transformed by analysis of a small number of genes, but uncertainty remains around critical nodes. Genomescale inferences so far have sampled a limited number of taxa and genes. Here we leveraged 144 genomes and 159 transcriptomes to investigate fish evolution with an unparalleled scale of data: >0.5 Mb from 1,105 orthologous exon sequences from 303 species, representing 66 out of 72 ray-finned fish orders. We apply phylogenetic tests designed to trace the effect of whole-genome duplication events on gene trees and find paralogy-free loci using a bioinformatics approach. Genome-wide data support the structure of the fish phylogeny, and hypothesis-testing procedures appropriate for phylogenomic datasets using explicit gene genealogy interrogation settle some long-standing uncertainties, such as the branching order at the base of the teleosts and among early euteleosts, and the sister lineage to the acanthomorph and percomorph radiations. Comprehensive fossil calibrations date the origin of all major fish lineages before the end of the Cretaceous.Fil: Hughes, Lily C.. National Museum of Natural History; Estados Unidos. The George Washington University; Estados UnidosFil: Ortí, Guillermo. National Museum of Natural History; Estados Unidos. The George Washington University; Estados UnidosFil: Huang, Yu. Beijing Genomics Institute; China. Chinese Academy of Sciences; República de ChinaFil: Sun, Ying. China National Genebank; China. Beijing Genomics Institute; ChinaFil: Baldwin, Carole C.. National Museum of Natural History; Estados UnidosFil: Thompson, Andrew W.. National Museum of Natural History; Estados Unidos. The George Washington University; Estados UnidosFil: Arcila, Dahiana. National Museum of Natural History; Estados Unidos. The George Washington University; Estados UnidosFil: Betancur, Ricardo. National Museum of Natural History; Estados Unidos. Universidad de Puerto Rico, Recinto de Rio Piedras; Puerto RicoFil: Li, Chenhong. Shanghai Ocean University; ChinaFil: Becker, Leandro Anibal. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Patagonia Norte. Instituto Andino Patagónico de Tecnologías Biológicas y Geoambientales. Universidad Nacional del Comahue. Instituto Andino Patagónico de Tecnologías Biológicas y Geoambientales.; Argentina. Universidad Nacional del Comahue. Centro Regional Universitario Bariloche; ArgentinaFil: Bellora, Nicolás. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Patagonia Norte. Instituto Andino Patagónico de Tecnologías Biológicas y Geoambientales. Universidad Nacional del Comahue. Instituto Andino Patagónico de Tecnologías Biológicas y Geoambientales.; Argentina. Universidad Nacional del Comahue. Centro Regional Universitario Bariloche; ArgentinaFil: Zhao, Xiaomeng. Chinese Academy of Sciences; República de China. Beijing Genomics Institute; ChinaFil: Li, Xiaofeng. Chinese Academy of Sciences; República de China. Beijing Genomics Institute; ChinaFil: Wang, Min. Beijing Genomics Institute; ChinaFil: Fang, Chao. Chinese Academy of Sciences; República de ChinaFil: Xie, Bing. Bgi-shenzhen; ChinaFil: Zhoui, Zhuocheng. China Fisheries Association; ChinaFil: Huang, Hai. Hainan Tropical Ocean University; ChinaFil: Chen, Songlin. Yellow Sea Fisheries Research Institute Chinese Academy Of Fishery Science; ChinaFil: Venkatesh, Byrappa. A-star, Institute Of Molecular And Cell Biology;Fil: Shi, Qiong. Chinese Academy of Sciences; República de Chin

Yellow- and green-cotyledon seeds of black soybean: Phytochemical and bioactive differences determine edibility and medical applications

Black soybean seed (BSS) is a traditional edible and medical food. The cotyledons of BSS are either yellow or green, but that difference's effect on functional and bioactivities are not clear. In the present study, the concentrations of the main functional components, including anthocyanins, isoflavones, fatty acids, protein, and polysaccharides, and in vitro antioxidant activities of yellow-cotyledon and green-cotyledon BSS (YBS and GBS, respectively) were compared. The anti-fatigue activities of the ethanol extract of BSS (EEB) were evaluated using mouse swimming endurance tests. Additionally, a metabolomics comparison between YBS and GBS was done using ultra-performance liquid chromatography coupled with quadrupole time-of-flight mass spectrometry (UPLC/Q-TOF MS) on high doses of EEB-treated mouse plasma. The results indicated that YBS showed significantly higher contents of anthocyanin and protein, and stronger antioxidant activity and anti-fatigue activity than GBS; while GBS showed higher levels of isoflavone, stearic acid, and polysaccharide. By infusing the feed with EEB, the swimming time of mice increased in a dose-dependent manner. The metabolomics results suggested that the anti-fatigue effect of EEB correlated well with serotonin and melatonin biosynthesis in vivo. All of the above results showed that BSS has anti-fatigue potential and might be used as a potential source of functional food ingredients.This study was financially supported by the National Natural Science Foundation of China (Grant No. 31971853) and the China Postdoctoral Science Foundation (Grant No. 2014 M560724 & 2017T100707).Peer reviewe

Effects of fine particulate matter (PM 2.5 ) on ovarian function and embryo quality in mice

Abstract(#br)Fine particulate matter (PM 2.5 ) has an adverse effect on reproductive function, in particular causing reduced male reproductive function, but relatively few studies have directly targeted its effects on female reproduction. To investigate the effects of PM 2.5 exposure on female reproduction, we exposed female mice to PM 2.5 by intratracheal instillation for 28 days, and evaluated apoptosis of ovarian granulosa cells and oocytes and the quality embryos after insemination. Our results showed increased numbers of apoptotic granulosa cells and oocytes after exposure to elevated concentrations of PM 2.5 , which had adverse effects on female fertility via compromising embryo development and quality. We conclude that PM 2.5 induced apoptosis of ovarian granulosa cells and oocytes leading to disrupted embryo development and female fertility in mice

Effects of fine particulate matter (PM2.5) on ovarian function and embryo quality in mice.

Fine particulate matter (PM2.5) has an adverse effect on reproductive function, in particular causing reduced male reproductive function, but relatively few studies have directly targeted its effects on female reproduction. To investigate the effects of PM2.5 exposure on female reproduction, we exposed female mice to PM2.5 by intratracheal instillation for 28 days, and evaluated apoptosis of ovarian granulosa cells and oocytes and the quality embryos after insemination. Our results showed increased numbers of apoptotic granulosa cells and oocytes after exposure to elevated concentrations of PM2.5, which had adverse effects on female fertility via compromising embryo development and quality. We conclude that PM2.5 induced apoptosis of ovarian granulosa cells and oocytes leading to disrupted embryo development and female fertility in mice