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Arnaud, L.

Publications and source records attributed to Arnaud, L..

3 recordsLinked to original sources

Threatened species bycatch hotspots in the tropical Atlantic Ocean

Predicting bycatch patterns in tropical tuna purse seine fisheries remain challenging due to low variance explained by existing models, limiting their use for management purposes. To address this limitation, we combined ecological network analyses and community detection methods to characterize recurring bycatch assemblages in tropical tuna purse seine fisheries. Ecological network analyses consistently revealed two key bycatch communities: one dominated by bony fishes with low conservation concern, and another by IUCN-listed threatened species (NT-CR; sharks, rays, sea turtles). By focusing on sets with high numbers of threatened species, we identified bycatch hotspots near Mauritania, Gabon and Angola. These hotspots result from seasonal fishing patterns and specific bycatch compositions, with specific composition in terms of sex and age, compared to the rest of the Atlantic. We suggest that the Mauritanian region is a potential candidate for shark nursery and sea turtle foraging grounds. These insights can guide the development of bycatch reduction strategies based on predictable spatio-temporal or community-specific features and provide a basis for targeted management actions.

ecology↗

LC3-associated phagocytosis is impaired in monocyte-derived macrophages from systemic sclerosis patients

Autophagy is a fundamental catabolic process performed by a network of autophagy related (ATG) proteins. Some ATG proteins coordinate parallel roles in so-called "noncanonical" autophagy such as LC3-associated phagocytosis (LAP). Both autophagy and LAP share key functions in immunity and inflammation and have been linked to autoimmune diseases. Systemic sclerosis (SSc) is an autoimmune disease of unknown etiology characterized by excessive fibrosis in skin and multiple internal organs linked with an aberrant immune activation. Several polymorphisms of genes coding for ATG proteins, particularly in ATG5, are more frequent in SSc patients. We hypothesized that autophagy and/or LAP could be dysregulated in immune cells from SSc patients. No defect of canonical autophagy was found in lymphocytes and monocytes isolated from peripheral blood mononuclear cells of SSc patients. We then generated monocyte-derived macrophages and performed phagocytosis assays to assess LAP activity. While M0 macrophage polarization appears similar than in healthy donors, we showed that LAP is downregulated in SSc patients. We now need to understand the molecular mechanisms underlying LAP dysregulations. Future investigations leading to the discovery of LAP modulating drugs could then open new therapeutic options for SSc treatment. Key messagesO_LIPolymorphisms of autophagy-related genes are associated with several autoimmune and autoinflammatory diseases, including SSc and SLE C_LIO_LIWhile autophagy has been shown to be dysregulated in circulating cells from SLE patients, no information is available for SSc C_LIO_LIWe show here that autophagy is comparable between PBMCs from patients and matched controls C_LIO_LIWe find a strong impartment of LAP, another ATG-dependent mechanism, in monocyte-derived macrophages from SSc patients C_LIO_LIAs LAP is involved in efferocytosis and the regulation of inflammation, we propose that restoring LAP activity could be a therapeutic option to limit fibrosis and inflammation C_LI

immunology↗

The Alzheimer's disease risk factor APOE4 drives pro-inflammation in human astrocytes via HDAC-dependent repression of TAGLN3

The Apolipoprotein E4 (APOE4) is the major allelic risk factor for late-onset Alzheimers disease (AD). APOE4 associates with a pro-inflammatory phenotype increasingly considered as critical in AD initiation and progression. Yet, the mechanisms driving an APOE4-dependent neuroinflammation remain unelucidated. Leveraging patient specific human induced Pluripotent Stem Cells (iPSCs) we demonstrate inflammatory chronicity and hyperactivated responses upon cytokines in human APOE4 astrocytes via a novel mechanism. We uncovered that APOE4 represses Transgelin 3 (TAGLN3), a new interacting partner of I{kappa}B, thus increasing the NF-kB activity. The transcriptional repression of TAGLN3 was shown to result from an APOE4-dependent histone deacetylase (HDAC) activity. The functional relevance of TAGLN3 was demonstrated by the attenuation of APOE4-driven neuroinflammation after TAGLN3 supplementation. Importantly, TAGLN3 downregulation was confirmed in the brain of AD patients. Our findings highlight the APOE4-TAGLN3 axis as a new pathogenic pathway that paves the way for the development of therapeutics to prevent maladaptive inflammatory responses in APOE4 carriers, while placing TAGLN3 downregulation as a potential biomarker of AD. GRAPHICAL ABSTRACT O_FIG O_LINKSMALLFIG WIDTH=98 HEIGHT=200 SRC="FIGDIR/small/440108v1_ufig1.gif" ALT="Figure 1"> View larger version (24K): org.highwire.dtl.DTLVardef@1036557org.highwire.dtl.DTLVardef@1f245bdorg.highwire.dtl.DTLVardef@c07c4aorg.highwire.dtl.DTLVardef@1200396_HPS_FORMAT_FIGEXP M_FIG C_FIG

neuroscience↗