Aldehydes and BTEX measurements and exposures in university libraries in Strasbourg (France).

International audienc

Tropospheric multiphase chemistry of 2,5- and 2,6-dimethylphenols: determination of the mass accommodation coefficients and the Henry's law constants.

International audienc

Specific accumulation of CYP94A1 transcripts after exposure to gaseous benzaldehyde: Induction of lauric acid ω-hydroxylase activity in Vicia sativa exposed to atmospheric pollutants

International audienc

Fluorescence Microscopy Analysis of Particulate Matter from Biomass Burning: Polyaromatic Hydrocarbons as Main Contributors

International audienceNew efficient approaches to the characterization of fly ash and particulate matter (PM) have to be developed in order to better understand their impacts on environment and health. Polycyclic aromatic hydrocarbons (PAH) contained in PM from biomass burning have been identified as genotoxic and cytotoxic, and some tools already exist to quantify their contribution to PM. Optical fluorescence microscopy is proposed as a rapid and relatively economical method to allow the quantification of PAH in different particles emitted from biomass combustion. In this study samples were collected in the flue gas of biomass-combustion facilities with nominal output ranging from 40 kW to 17.3 MW. The fly ash samples were collected with various flue gas treatment devices (multicyclone, baghouse filter, electrostatic precipitator); PM samples were fractionated from the flue gas with a DEKATI® DGI impactor. A method using fluorescence observations (at 470 nm), white-light observations and image processing has been developed with the aim of quantifying fluorescence per sample. Organic components of PM and fly ash, such as PAH, humic-like substances (HULIS) and water-soluble organic carbon (WSOC) were also quantified. Fluorescence microscopy analysis method assessment was first realized with fly ash that was artificially coated with PAH and HULIS. Total amounts of PAH in the three size fractions of actual PM from biomass burning strongly correlated with the intensities of fluorescence. These encouraging results contribute to the development of a faster and cheaper method of quantifying particle-bound PAH

The PLA2R1-JAK2 pathway upregulates ERRα and its mitochondrial program to exert tumor-suppressive action

Little is known about the biological role of the phospholipase A2 receptor (PLA2R1) transmembrane protein. In recent years, PLA2R1 has been shown to have an important role in regulating tumor-suppressive responses via JAK2 activation, but the underlying mechanisms are largely undeciphered. In this study, we observed that PLA2R1 increases the mitochondrial content, judged by increased levels of numerous mitochondrial proteins, of the mitochondrial structural component cardiolipin, of the mitochondrial DNA content, and of the mitochondrial DNA replication and transcription factor TFAM. This effect of PLA2R1 relies on a transcriptional program controlled by the estrogen-related receptor alpha1 (ERRα) mitochondrial master regulator. Expression of ERRα and of its nucleus-encoded mitochondrial targets is upregulated upon PLA2R1 ectopic expression, and this effect is mediated by JAK2. Conversely, downregulation of PLA2R1 decreases the level of ERRα and of its nucleus-encoded mitochondrial targets. Finally, blocking the ERRα-controlled mitochondrial program largely inhibits the PLA2R1-induced tumor-suppressive response. Together, our data document ERRα and its mitochondrial program as downstream effectors of the PLA2R1-JAK2 pathway leading to oncosuppression

Lysyl oxidase activity regulates oncogenic stress response and tumorigenesis

International audienceCellular senescence, a stable proliferation arrest, is induced in response to various stresses. Oncogenic stress-induced senescence (OIS) results in blocked proliferation and constitutes a fail-safe program counteracting tumorigenesis. The events that enable a tumor in a benign senescent state to escape from OIS and become malignant are largely unknown. We show that lysyl oxidase activity contributes to the decision to maintain senescence. Indeed, in human epithelial cell the constitutive expression of the LOX or LOXL2 protein favored OIS escape, whereas inhibition of lysyl oxidase activity was found to stabilize OIS. The relevance of these in vitro observations is supported by in vivo findings: in a transgenic mouse model of aggressive pancreatic ductal adenocarcinoma (PDAC), increasing lysyl oxidase activity accelerates senescence escape, whereas inhibition of lysyl oxidase activity was found to stabilize senescence, delay tumorigenesis, and increase survival. Mechanistically, we show that lysyl oxidase activity favors the escape of senescence by regulating the focal-adhesion kinase. Altogether, our results demonstrate that lysyl oxidase activity participates in primary tumor growth by directly impacting the senescence stability