Litcius/Paper detail

Persistent JunB activation in fibroblasts disrupts stem cell niche interactions enforcing skin aging

Pallab Maity, Karmveer Singh, Linda Krug, Albert Koroma, Adelheid Hainzl, Wilhelm Bloch, Stefan Kochanek, Meinhard Wlaschek, Marina Schorpp‐Kistner, Peter Angel, Anita Ignatius, Hartmut Geiger, Karin Scharffetter‐­Kochanek

2021Cell Reports57 citationsDOIOpen Access PDF

Abstract

and repression of insulin growth factor-1 (IGF-1), initiates the installment of fibroblast senescence. Fibroblast senescence profoundly disrupts the metabolic and structural niche, and its essential interactions with different stem cells thus enforces depletion of stem cells pools and skin tissue decline. In fact, silencing of JunB in a fibroblast-niche-specific manner-by reinstatement of IGF-1 and p16 levels-restores skin stem cell pools and overall skin tissue integrity. Here, we report a role of JunB in the control of connective tissue niche and identified targets to combat skin aging and associated pathologies.

Topics & Concepts

JUNBCell biologyStem cellBiologySenescenceFibroblastTranscription factorConnective tissueImmunologyCell cultureGeneticsGeneSkin Protection and AgingTelomeres, Telomerase, and Senescencemelanin and skin pigmentation