The epidermis is the barrier that keeps water in and the world out. It is being renewed continuously: new cells arise at the base, travel up, mature, and perform their final sacrificial act. They flatten, lose their nucleus, and die to deposit their dense keratin filaments forming interlocking bricks that seal the surface. In congenital skin diseases, the wall cracks: painful, visible, lifelong, often incurable. Understanding how specific mutations undermine the barrier is the first step toward repair.
reNEW research
In Karine Raymond’s group at reNEW Leiden we grow skin organoids from human induced pluripotent stem cells carrying mutations associated with skin diseases to study their impact on the skin formation and maintenance. We also isolate and expand keratinocytes, the main cell type of the epidermis, to further characterise the intrinsic effects of these mutations and determine how they alter the cells’ ability to sense and adapt to environmental stress.
Image description
The outer layer of a reconstructed epidermis stained for filaggrin, responsible for the formation of the keratin filaments.
Credits
Victor Lorrain, research technician, Raymond lab, reNEW Leiden.
