Abstract
The human interfollicular epidermis is renewed throughout life by populations of proliferating basal keratinocytes. Though interfollicular keratinocyte stem cells have been identified, it is not known how self-renewal in this compartment is spatially organized. At the epidermal-dermal junction, keratinocytes sit atop a heterogeneous mix of dermal cells that may regulate keratinocyte self-renewal by influencing local tissue architecture and signalling microenvironments. Focusing on the rete ridges and complementary dermal papillae in human skin, we review the identity and organisation of abundant dermal cells types and present evidence for interactions between the dermal microenvironment and the interfollicular keratinocytes.
Highlights
Skin is a large, complex organ that is constantly renewed throughout life
The interfollicular epidermis is arranged in a spatial hierarchy with cells becoming more differentiated as they move to the outer layers and eventually shed
There is much to be learnt about how changes in the tissue microenvironment establish and modulate the organisation of keratinocyte populations to achieve sustained self-renewal
Summary
Complex organ that is constantly renewed throughout life. The interfollicular epidermis is arranged in a spatial hierarchy with cells becoming more differentiated as they move to the outer layers and eventually shed. A population of slow cycling cells, previously shown to express high levels of β-1 integrin and to possess the properties of stem cells [22,23], is likely located in regions of high beta-1 integrin expression at the tip of the dermal papillae These findings suggest that keratinocyte renewal may involve a complex movement of cells laterally and down the rete ridge, as well as along the basal-apical axis to maintain tissue architecture. The sites of high β-1 expression appear to be body site specific: at the tip of the dermal papillae in breast, foreskin and scalp, but at the tip of the deep rete ridge in palm and foot skin [21,22] The basis for this is unknown, but suggests that keratinocyte self-renewal may be organised around local differences in tissue architecture that are yet to be determined. As more precise ways to define tissue architecture or dermal cell populations are developed, it may be possible to identify extrinsic factors that account for the spatial organisation of keratinocyte self-renewal
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