The skin integrity can be disrupted by changes of the tissue microenvironment but also by systemic modifications of the body homeostasis. In this research axis, we decipher the mechanisms of skin’s weakening in various contexts of micro-environmental insults. We are particularly focusing on chronological aging and associated pathological conditions such as type 2 diabetes. All of the skin cells such as keratinocytes, fibroblasts, vascular cells, macrophages, and adipocytes have a capacity to communicate between themselves within the different tissue layers and interact with their environment. We thus study how the mechanisms identified in the first axis will be modulated in the aged skin, from the molecular regulations (exerted for instance by ncRNA) to the tissue functions. In addition, type 2 diabetes is a pathological condition that develops with aging and is often associated to overweight or obesity. We aim to clarify the role of dermal white adipose tissue in regulating dermal function depending on their inflammatory status and more specifically their effect on elastogenesis triggered by fibroblasts.

Participants: G Aimond, C Bonod, F Chevalier, R Debret, L Dubourg, B Fromy, A Josset-Lamaugarny, J Lamartine, M Lo, KL Liu,  N Picard, D Sigaudo-Roussel, J Vial

Collaborations: A Thépot (LabSkinCreation), P Baril (CNRS Tours), M Kasper (Karolinska Institute), JC Lecron (Poitiers), L Misery (LIEN Brest), M Vickers (Liggins Institute,NZ), L Baptista (Federal University of Rio de Janeiro, Brazil), G. Crambert (CNRS Paris), C. Hübner (Universität Klinikum Jena, Allemagne), D. Eladari and R. Chambert (INSERM, La Réunion), J. Sethi (Univ of Southampton).

Fundings: ANR TRIP, ANR Prostarget, ANR ConTarKid, Allergan, BIKE INFINITUS, Urgo Karite, PHRC HCL