Podoplanin shapes epidermal morphogenesis and coordinates stem cell and epidermal-dermal responses during inflammatory remodelling

Keratinocyte-expressed podoplanin loss in mice causes basal layer disorganization, altered division orientation, and increased epidermal thickness, uncoupling differentiation marker expression from barrier maturation.

• Why it matters: Epidermal development and inflammatory remodelling require keratinocytes to coordinate differentiation with tissue architecture and functional barrier acquisition, but how podoplanin contributes to this coupling is unclear.
• What they did: Using global podoplanin deletion and K5Cre-driven basal keratinocyte deletion, the study tracked epidermal morphogenesis, differentiation markers, barrier acquisition, junctional actin organization, ERM phosphorylation, and TPA responses.
• The result: Barrier function recovered despite persistent histological abnormalities; in primary keratinocytes, podoplanin deficiency reduced ERM phosphorylation and junctional pERM/ppMLC2 enrichment, and in adult skin it prevented TPA-linked BrdU-retaining cell changes.

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