Amazing stuff!
"Key points
- The skin has an amazing ability to regenerate and heal.
- Researchers have uncovered one of the earliest steps in how skin stem cells learn to repair tissue.
- The findings could inform the development of skin healing methods, including for organ repair and skin transplants.
...
discovered that, during the earliest stages of embryonic development, skin stem cells contribute to forming a protective skin layer that accelerates healing as the embryo grows.
Their findings reveal one of the earliest steps in how skin stem cells learn to repair tissue ...
The researchers examined development in zebrafish embryos, the skin organization of which is similar to human embryos. Specifically, they analyzed the thin transparent layer of cells that lines the zebrafish fin folds in the embryo, structures that transition into fins during development in a process that’s similar to limb development in mammals. ...
compared their findings in the embryonic zebrafish fin fold to a bilayer model of the human epidermis. Their modeling revealed that collagen and laminin matrices similarly influence human skin cells. Specifically, they found that laminin inhibited the proteins that drive desmosome junction formation. ..."
From the abstract:
"Epidermal stem cells interact with the extracellular matrix (ECM) to regulate their differentiation and maintain skin architecture.
Here, we demonstrate a role for basal epidermal stem cells (BECs)-ECM interaction in regulating adhesion molecules expressed by the periderm—the superficial epidermal cells (SECs) of the embryonic bilayered skin.
Using the developing zebrafish fin fold, we identify BECs form distinct regions of collagen- versus laminin- enriched basement membranes through integrin-mediated adhesions.
Mechanistically, collagen-associated BECs form desmosomes and adherens junctions (AJs) with SECs while laminin-associated BECs display reduced desmosomes but sustain AJs and actomyosin expression with SECs.
Notably, we show both in vivo and in a bilayered human keratinocyte model, that laminin, compared to collagen, is sufficient to repress desmosome formation while sustaining AJs specifically at the interlayer cell contacts.
In vivo, laminin deficiency enhances desmosome expression across layers and impairs the wound-healing capacity of SECs. This defect was partially rescued by genetic reduction of the desmosome protein Desmoplakin-1a, highlighting the role of ECM-dependent junctional specialization in mediating differences in SEC injury response.
Overall, our findings identify that stem cells, through their matrix, establish specialized junctions in the overlying stratified epithelium, which contribute to skin healing properties."
Epidermal stem cells control periderm injury repair via matrix-driven specialization of intercellular junctions (open access)
Fig. 1: Region-Specific Junctional and Cytoskeletal Organization of BECs in the Fin Fold.
No comments:
Post a Comment