Since the crucial role of the microenvironment has been highlighted, many studies have been focused on the role of biomechanics in cancer cell growth and the invasion of the surrounding environment. Despite the search in recent years for molecular biomarkers to try to classify and stratify cancers, much effort needs to be made to take account of morphological and nanomechanical parameters that could provide supplementary information concerning tissue complexity adaptation during cancer development. The biomechanical properties of cancer cells and their surrounding extracellular matrix have actually been proposed as promising biomarkers for cancer diagnosis and prognosis. The present review first describes the main methods used to study the mechanical properties of cancer cells. Then, we address the nanomechanical description of cultured cancer cells and the crucial role of the cytoskeleton for biomechanics linked with cell morphology. Finally, we depict how studying interaction of tumor cells with their surrounding microenvironment is crucial to integrating biomechanical properties in our understanding of tumor growth and local invasion.
Due to the expansion of the ageing population, understanding age-related pathologies remains of great interest. The human skin is particularly affected by environmental stressors and goes through profound alterations that modify its appearance throughout ageing (for review, [1]). These modifications occur in the epidermis that becomes thinner due to reduced capacities in proliferation/differentiation, resulting in reduction of exchange surface. The alterations also arise in the dermis where the number of fibroblasts declines, leading to a decrease in collagen and elastin fibres of the extracellular matrix. This process of reduced proliferation abilities of cells including keratinocytes in the epidermis and fibroblasts in the dermis is mainly due to cellular senescence. These modifications are due to chronologically intrinsic ageing, which can also be amplified by extrinsic factors such as solar UV radiation. Even if the molecular mechanisms underlying human skin ageing are increasingly understood, it remains essential to understand skin homeostasis and its perturbation during ageing process in an integrated view.
Dans le cadre du module d’enseignement Communication Scientifique et Littérature du Master Biologie Moléculaire et Cellulaire de Lyon, les étudiants des parcours M2 Génopath et Biologie de la Peau se sont formés à l’écriture scientifique sur un sujet libre. Suite à un travail préparatoire avec l’équipe pédagogique, chaque étudiant a rédigé, conseillé par un chercheur, une Nouvelle.
Le parcours M2 Génopath s’adresse aux étudiants scientifiques et médecins et les forme à la recherche fondamentale dans les domaines de la génétique, de la biologie cellulaire et de leurs applications biomédicales. Le parcours M2 Biologie de la Peau est une formation unique en France, et forme des spécialistes de la recherche en biologie cutanée qui s’inséreront dans les services de recherche et développement hospitalier ou de l’industrie dermo-cosmétique et dermo-pharmaceutique.
Chronic leg ulcers are a major health burden globally, increasing in incidence with ageing and morbidity from diabetes. A common mechanism highlighted in chronic hard to heal wounds is exaggerated and sustained inflammation which inhibits the closure and therefore represents a therapeutic target. In the present study, we analyzed the effect of supernatant extracted from two strains of Faecalibacterium prausnitzii, a commensal gut microbiome known to have anti-inflammatory activity. C57BL/6 wild type mice were subjected to full thickness excisional wounds and randomized for treatment by extracts from SPA2 or SPAH strains versus vehicle control. Four days post wounding there was a dramatic and significant reduction of nuclear p65 staining in wounds reflecting inhibition of NFkB activation. This was accompanied by a decline in proinflammatory cytokines, il12p35 or tnfa. Although the bacterial supernatants did not significantly affect the myeloid immune infiltrate, wound closure was significantly accelerated, as well as collagen and myofibroblast-related gene expression. To further understand the specificity of this effect on NFkB signalling we used pharmacological inhibitor of IKK and NFkB activation versus an inhibitor of the inflammasome (NLRP3). NFkB inhibition resulted in similar acceleration of wound closure however inhibition of the inflammasome did not affect closure. In conclusion, supernatant from specific strains derived from F. prausnitzii can regulate wound inflammation through the NFkB pathway and accelerate wound closure through increased myofibroblast differentiation and collagen deposition. This finding might open new therapeutic avenues for chronic hyperinflammatory diabetic or venous ulcers.
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