Human epidermal keratinocytes upregulate expression of the prolactin receptor after the onset of terminal differentiation, but do not respond to prolactin.

@article{Poumay1999HumanEK,
  title={Human epidermal keratinocytes upregulate expression of the prolactin receptor after the onset of terminal differentiation, but do not respond to prolactin.},
  author={Yves Poumay and Genevi{\`e}ve Jolivet and Mark R. Pittelkow and Françoise Herphelin and I Y De Potter and Vanio Ivanov Mitev and Louis Marie Houdebine},
  journal={Archives of biochemistry and biophysics},
  year={1999},
  volume={364 2},
  pages={
          247-53
        }
}
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… 
Human scalp hair follicles are both a target and a source of prolactin, which serves as an autocrine and/or paracrine promoter of apoptosis-driven hair follicle regression.
TLDR
The data suggest that PRL acts as an autocrine hair growth modulator with catagen-promoting functions and that the hair growth-inhibitory effects of PRL demonstrated here may underlie the as yet ill-understood hair loss in patients with hyper-prolactinemia.
High-cell-density phorbol ester and retinoic acid upregulate involucrin and downregulate suprabasal keratin 10 in autocrine cultures of human epidermal keratinocytes.
TLDR
In this report, the phenotype of autocrine keratinocytes was studied at high cell density (postconfluence), specifically after treatment with 12-O-tetradecanoylphorbol 13-acetate (TPA), or all-trans retinoic acid (RA), which simulates for the first time the in vivo effects of RA.
Human EGF receptor (HER) family and heregulin members are differentially expressed in epidermal keratinocytes and modulate differentiation.
TLDR
Together, HER2, HER3, and heregulin constitute a potential autocrine-paracrine system involved in epidermal homeostasis and repair, as well as in hyperproliferative pathologies.
Prolactin and the skin: a dermatological perspective on an ancient pleiotropic peptide hormone.
TLDR
It is argued that systematic exploration of the "PRL-skin connection" will fertilize the development of previously unreported neuroendocrinological strategies for managing selected skin disorders, and identify potential therapeutic targets for the management of these skin disorders.
Prolactin signaling influences the timing mechanism of the hair follicle: analysis of hair growth cycles in prolactin receptor knockout mice.
TLDR
It is demonstrated that PRL has an inhibitory effect on murine hair cycle events, and this study shows that messenger RNA transcripts encoding the one long and two short forms of PRL receptor are present in the skin of adult and neonate mice.
STAT5a/PPARgamma pathway regulates involucrin expression in keratinocyte differentiation.
TLDR
Early evidence is provided of a major role for STAT5a in the differentiation of keratinocytes, where it contributes to involucrin expression by activating the PPARgamma signal.
Interplay Between Prolactin and Pathogenesis of Psoriasis Vulgaris.
TLDR
This theory/concept that PRL acts as a neuroendocrine modulator of both skin epithelial growth and the skin immune system can be integrated into current views on the multilevel neuro endocrine- immune communication along the brain-skin axis in health and disease.
Regulation of epidermal homeostasis and repair by phosphoinositide 3-kinase
The epidermis undergoes continuous self-renewal to maintain its protective function. Whereas growth factors are known to modulate overall skin homeostasis, the intracellular signaling pathways, which
Meaning of relative gene expression in multilayered cultures of epidermal keratinocytes
TLDR
This study illustrates that comparing the relative expression level of mRNAs to that of a basal layer‐specific gene (e.g. ITGA6) better illustrates the contribution of specific differentiation markers to the process of epidermal morphogenesis.
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The pituitary hormone prolactin is extended to include regulation of in vitro proliferation of human keratinocytes, and the possibility of a completely defined growth medium for keratinocyte culture is suggested.
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It is shown that prolactin acts as a direct growth and differentiation factor for human prostate, as measured by changes in DNA synthesis and epithelial morphology of organ cultures, and the existence of an autocrine/paracrine loop of Prolactin in the human prostate is supported.
Human dermal fibroblast cells express prolactin in vitro.
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The synthesis and release of prolactin (PRL) from dermal fibroblasts in vitro is demonstrated, suggesting a potential local source of PRL in skin, and steroids and PGE2 together were synergistic, reaching maximal values of approximately 10 ng/72 h after 2 or more weeks of treatment.
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It is demonstrated that MGF is rapidly activated by PRL alone or by human growth hormone, a natural ligand of many PRL receptors (PRL-Rs), in the cytoplasm and accumulated in the nucleus.
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TLDR
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TLDR
It is suggested that the 95 kDa protein is a likely novel mitogen for keratinocytes, which is unrelated to prolactin and showed high homology with a bovine 90 kDa heat shock protein in the limited sequencing of an internal peptide.
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