Human Epidermal Keratinocytes Upregulate Expression of the Prolactin Receptor after the Onset of Terminal Differentiation, but Do Not Respond to Prolactin

Growing and differentiating keratinocytes maintain the epidermal barrier. This is partly controlled by growth factors and hormones. Prolactin (PRL) is named after its hormonal role in mammals during lactation, but is found in all vertebrates where PRL exerts various effects. In serum-free keratinocyte cultures, PRL was thought to be the factor responsible for the proliferative effect of bovine pituitary extract. Here, we evaluated PRL as a clonogenic factor for keratinocytes and found no mitogenic activity. Studying the expression of the PRL receptor by keratinocytes, we found the receptor upregulated only after culture confluence, in differentiating keratinocytes, but we were unable to detect any cellular response to PRL. The hormone does not alter the gene expression of either early (suprabasal keratin) or late (involucrin) differentiation markers by keratinocytes. Accordingly, no activation of the transcription factor Stat5 by PRL can be detected in keratinocytes, Stat5 being nevertheless detected by Western blot.