Multiscale Structure of Starches Grafted with Hydrophobic Groups: A New Analytical Strategy.

Starch, an abundant and low-cost plant-based glucopolymer, has great potential to replace carbon-based polymers in various materials. In order to optimize its functional properties for bioplastics applications chemical groups need to be introduced on the free hydroxyl groups in a controlled manner, so an understanding of the resulting structure-properties relationships is therefore essential. The purpose of this work was to study the multiscale structure of highly-acetylated (degree of substitution, 0.4 < DS ≤ 3) and etherified starches by using an original combination of experimental strategies and methodologies. The molecular structure and substituents repartition were investigated by developing new sample preparation strategies for specific analysis including Asymmetrical Flow Field Flow Fractionation associated with Multiangle Laser Light Scattering, Nuclear Magnetic Resonance (NMR), Raman and Time of Flight Secondary Ion Mass spectroscopies. Molar mass decrease and specific ways of chain breakage due to modification were pointed out and are correlated to the amylose content. The amorphous structuration was revealed by solid-state NMR. This original broad analytical approach allowed for the first time a large characterization of highly-acetylated starches insoluble in aqueous solvents. This strategy, then applied to characterize etherified starches, opens the way to correlate the structure to the properties of such insoluble starch-based materials.

Aldosterone up-regulates MMP-9 and MMP-9/NGAL expression in human neutrophils through p38, ERK1/2 and PI3K pathways.

Aldosterone and mineralocorticoid receptors are important regulators of inflammation. During this process, chemokines and extracellular matrix degradation by matrix metalloproteases, such as MMP-9, help leukocytes reaching swiftly and infiltrating the injured tissue, two processes essential for tissue repair. Leukocytes, such as neutrophils, are a rich source of MMP-9 and possess mineralocorticoid receptors (MR). The aim of our study was to investigate whether aldosterone was able to regulate proMMP-9, active MMP-9 and MMP-9/NGAL production in human neutrophils. Here we show that aldosterone increased MMP-9 mRNA in a dose- and time-dependent manner. This hormone up-regulated also dose-dependently proMMP-9 and active MMP-9 protein release as well as the MMP-9/NGAL protein complex. PI3K, p38 and ERK1/2 inhibition diminished these aldosterone-induced neutrophil productions. Furthermore, spironolactone, a MR antagonist, counteracted aldosterone-induced increases of proMMP-9, active MMP-9 and MMP-9/NGAL complex. These findings indicate that aldosterone could participate in tissue repair by modulating neutrophil activity and favoring extracellular matrix degradation.

Aldosterone increases VEGF-A production in human neutrophils through PI3K, ERK1/2 and p38 pathways.

Aldosterone is now recognised as an important actor in inflammation processes. Neoangiogenesis plays a crucial role in this complex process and immune cells, such as neutrophils, appear to be able to secrete different forms of (pro)angiogenic molecules, especially VEGF-A. The present work was undertaken to investigate whether aldosterone was able to regulate VEGF-A production in human neutrophils. The HL-60 (progranulocytic) cell line and human polymorphonuclear leukocytes were incubated for different time periods with aldosterone. Total cellular RNA extraction, submitted to reverse transcription and real time semi-quantitative PCR, was used to study VEGF-A mRNA expression. Cell supernatants were collected and ELISA tests were performed to analyse VEGF-A protein production. Aldosterone increased VEGF-A mRNA and protein expression in a dose- and time-dependent manner in both cell types. Inhibitors of PI3 kinases, ERK1/2, and to a lesser extent of p38 MAPK, decreased this aldosterone-induced immune cell activation. Western-blot performed with HL-60 cells confirmed that ERK1/2 and p38 MAPK pathways were stimulated by aldosterone. Mineralocorticoid receptors are implicated in this VEGF-A up-regulation because HL-60 cells pre-treated with spironolactone, an aldosterone receptor antagonist, diminished the effects of aldosterone. Aldosterone was also able to increase VEGF-A production of phagocytic cells such as neutrophils. These results suggest that this hormone could play an active role in the neovascularisation process by favouring entry of plasma proteins and fluids into the vascular wall, cell proliferation and tissue rebuilding.