Biology subjects

Bertrand, L.

Publications and source records attributed to Bertrand, L..

3 recordsLinked to original sources

bioRxiv2020

Beta-3 Adrenoreceptors protect from hypertrophic remodelling through AMP-Activated Protein Kinase and Autophagy.

AimsThe abundance of beta3-adrenergic receptors ({beta}3-ARs) is upregulated in diseased human myocardium. We previously showed that cardiac-specific expression of {beta}3-AR inhibits the hypertrophic response to neurohormonal stimulation. Here, we further analyzed signalling pathways involved in the anti-hypertrophic effect of {beta}3-AR. MethodsIn vitro hypertrophic responses to phenylephrine (PE) were analyzed in neonatal rat ventricular myocytes (NRVM) infected with a recombinant adenovirus expressing the human {beta}3-AR (AdVh{beta}3). We confirmed results in mice with cardiomyocyte-specific moderate expression of human {beta}3-AR ({beta}3-TG) and WT littermates submitted to thoracic transverse aortic constriction (TAC) for 9 weeks. ResultsWe observed a colocalization of {beta}3-AR with the AMP-activated protein kinase (AMPK) both in neonatal rat andin adult mouse cardiomyocytes. Treatment of NRVM with PE induced hypertrophy and a decrease in phosphorylation of Thr172-AMPK (/2, p=0.0487) and phosphorylation of Ser79- acetyl-CoA carboxylase (ACC) (/2.6, p=0.0317), inducing an increase in phosphorylated Ser235/236 S6 protein (x2.5, p=0.0367) known to be involved in protein synthesis. These effects were reproduced by TAC in WT mice, but restored to basal levels in {beta}3-AR expressing cells/mice. siRNA targeting of AMPK partly abrogated the anti-hypertrophic effect of {beta}3-AR in response to PE in NRVM (x1.3, p<0.0001). Concomitant with hypertrophy, autophagy measured by microtubule-associated protein 1 light chain 3 (LC3)-II/LC3-I ratio and p62 abundance was decreased by PE in NRVM (/2.6, p=0.0010 and x3, p=0.0016, respectively) or TAC in WT mice (/5.4, p=0.0159); and preserved in human {beta}3-AR expressing cells and mice, together with reduced hypertrophy. ConclusionsCardiac-specific moderate expression of {beta}3-AR inhibits the hypertrophic response in part through AMPK activation followed byinhibition of protein synthesis and preservation of autophagy. Activation of the cardiac {beta}3-AR pathway may provide future therapeutic avenues for the modulation of hypertrophic remodelling.

cell biology↗

bioRxiv2019

Different salicylic and jasmonic acids imbalances are involved in the oxidative stress-mediated cell death, induced by fumonisin B1 in maize seedlings with contrasting resistance to Fusarium verticillioides ear rot in the field.

Background and aimFungal and plant secondary metabolites modulate the plant-pathogen interactions. However, the participation of fumonisins in the Fusarium verticillioides-maize pathosystem is unclear. In this work was studied the cell death, and the reactive oxygen species (ROS) - phytohormone imbalance interplay underlying the phytotoxicity of fumonisin B1 (FB1) in maize germplasms with contrasting resistance to Fusarium ear rot in the field. MethodsResistant (RH) and susceptible hybrid (SH) maize seedlings, grown from uninoculated seeds irrigated with FB1 (1 and 20 ppm), were harvested at 7, 14 and 21 days after planting, and were examined for electrolyte leakage (aerial parts); and for oxidative stress biomarkers (aerial parts and roots). The phytohormone (salicylic and jasmonic acids) imbalance interplay underlying the FB1-induced cell death were further explored in seedlings exposed 24 h to the mycotoxin (1 ppm) in hydroponics. ResultsCell death increased in RH and SH watered with 1 and 20 ppm of mycotoxin, respectively. Both toxin concentrations were pro-oxidant, and the major perturbations were found in roots. An Integrated Biomarker Response index was calculated suggesting that phytotoxicity occurs in a redox context more efficiently controlled by RH. ConclusionThe pre-treatment with the antioxidant ascorbic acid led to the conclusion that cell death in RH was related to a salicylic acid increase mediated by ROS. Nevertheless, FB1 induced two different phytohormonal regulatory mechanisms mediated by oxidative stress in both maize hybrids.

plant biology↗

bioRxiv2019

Proteolysis and neurogenesis modulated by LNR domain proteins explosion support male differentiation and sacrificial behaviour in the iteroparous crustacean Oithona nana.

Copepods are the most numerous animals and play an essential role in the marine trophic web and biogeochemical cycles. The genus Oithona is described as having the highest numerical density, as the most cosmopolite copepod and iteroparous. The Oithona male paradox obliges it to alternate feeding (immobile) and mating (mobile) phases. As the molecular basis of this trade-off is unknown, we investigated this sexual dimorphism at the molecular level by integrating genomic, transcriptomic and protein-protein interaction analyses.\n\nWhile a ZW sex-determination system was predicted in O. nana, a fifteen-year time-series in the Toulon Little Bay showed a biased sex ratio toward females (male / female ratio < 0.15{+/-}0.11) highlighting a higher mortality in male. Here, the transcriptomic analysis of the five different developmental stages showed enrichment of Lin12-Notch Repeat (LNR) domains-containing proteins coding genes (LDPGs) in male transcripts. The male also showed enrichment in transcripts involved in proteolysis, nervous system development, synapse assembly and functioning and also amino acid conversion to glutamate. Moreover, several male down-regulated genes were involved in the increase of food uptake and digestion. The formation of LDP complexes was detected by yeast two-hybrid, with interactions involving proteases, extracellular matrix proteins and neurogenesis related proteins.\n\nTogether, these results suggest that the O. nana male hypermotility is sustained by LDP-modulated proteolysis allowing the releases and conversions of amino acid into the excitatory neurotransmitter glutamate. This process could permit new axons and dendrites formation suggesting a sexual nervous system dimorphism. This could support the hypothesis of a sacrificial behaviour in males at the metabolic level.

molecular biology↗