Localisation of receptors for prolactin in ovine skin

Choy, V. J.; Nixon, A. J.; Pearson, A J

doi:10.1677/joe.0.1440143

Cited by 23 publications

(12 citation statements)

References 24 publications

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“…Although PRL protein expression in murine hair follicles has not been previously reported, other studies have shown that PRLR RNA is localized in the epidermis, skin glands, ORS, and DP of ovine anagen hair follicles. 34,35,47 In contrast to studies in sheep, we could detect the PRLR only in follicular epithelial cells and it was notably absent from the DP, connective tissue sheath, and sebaceous gland. These findings were partially consistent with those of Craven and colleagues, 15 who found PRLR staining in the epidermis, sebaceous gland, and ORS of the hair follicle, but not in the DP of murine anagen hair follicles.…”

Section: Discussioncontrasting

confidence: 99%

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Prolactin and Its Receptor Are Expressed in Murine Hair Follicle Epithelium, Show Hair Cycle-Dependent Expression, and Induce Catagen

Foitzik

Krause

Nixon

et al. 2003

The American Journal of Pathology

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Here, we provide the first study of prolactin (PRL) and prolactin receptor (PRLR) expression during the nonseasonal murine hair cycle, which is, in contrast to sheep, comparable with the human scalp and report that both PRL and PRLR are stringently restricted to the hair follicle epithelium and are strongly hair cycle-dependent. In addition we show that PRL exerts functional effects on anagen hair follicles in murine skin organ culture by down-regulation of proliferation in follicular keratinocytes. In telogen follicles, PRL-like immunoreactivity was detected in outer root sheath (ORS) keratinocytes. During early anagen (III to IV), the developing inner root sheath (IRS) and the surrounding ORS were positive for PRL. In later anagen stages, PRL could be detected in the proximal IRS and the inner layer of the ORS. The regressing (catagen) follicle showed a strong expression of PRL in the proximal ORS. In early anagen, PRLR immunoreactivity occurred in the distal part of the ORS around the developing IRS, and subsequently to a restricted area of the more distal ORS during later anagen stages and during early catagen. The dermal papilla (DP) stayed negative for both PRL and PRLR throughout the cycle. Telogen follicles showed only a very weak PRLR staining of ORS keratinocytes. The long-form PRLR transcript was shown by real-time polymerase chain reaction to be transiently down-regulated during early anagen, whereas PRL transcripts were up-regulated during mid anagen. Addition of PRL (400 ng/ml) to anagen hair follicles in murine skin organ culture for 72 hours induced premature catagen development in vitro along with a decline in the number of proliferating hair bulb keratinocytes. These data support the intriguing concept that PRL is generated locally in the hair follicle epithelium and acts directly in an autocrine or paracrine manner to modulate the hair cycle. Hair follicles are unusual in that they undergo lifelong cycles of growth and regression. Active hair growth (anagen) is accompanied by hair shaft elongation, melanogenesis, and by massive keratinocyte proliferation, whereas hair follicle regression (catagen) is characterized by terminal differentiation and apoptosis, resulting in the resting stage (telogen) and in hair shaft shedding (exogen). The molecular mechanisms that are responsible for this tightly controlled process are still not clear, but in the last decade a large, yet limited number of growth factors, cytokines, neuropeptides, neurotransmitters, and hormones have been shown to play important regulatory roles.1-3 A particularly intriguing issue in this context is the search for the set of locally generated hormones and neurotrophines that are involved in that growth control 4,5 beyond the well-recognized effects of locally metabolized steroid hormones.

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Section: Discussioncontrasting

confidence: 99%

“…31 And although PRL is incapable of binding to the receptors for GH, it has somatotrophic activity in rodents. 32 PRLRs have been shown to be expressed in epidermal keratinocytes in humans, 33 in the wool follicles of sheep, 34,35 and anagen hair follicles of mice 15 suggesting that PRL operates directly on the skin.…”

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Prolactin and Its Receptor Are Expressed in Murine Hair Follicle Epithelium, Show Hair Cycle-Dependent Expression, and Induce Catagen

Foitzik

Krause

Nixon

et al. 2003

The American Journal of Pathology

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“…These in situ hybridisation data concur with earlier receptor protein localisation (Choy et al 1995(Choy et al , 1997). As noted above, migration of clonogenic cells from the outer root sheath has been implicated in cycle control (Oshima et al 2001).…”

Section: Discussionsupporting

confidence: 90%

“…Fibre growth can be altered by either local injection (Thomas et al 1994) or systemic prolactin treatments (Pearson et al 1999). Prolactin receptors (PRLR) have been detected in skin by in situ hybridisation (Ouhtit et al 1993), radioligand binding (Choy et al 1995) and immunocytochemistry (Choy et al 1997, Craven et al 2001. Interestingly, PRLR localise particularly to the outer root sheaths and dermal papillae of hair follicles.…”

Section: Introductionmentioning

confidence: 99%

Regulation of prolactin receptor expression in ovine skin in relation to circulating prolactin and wool follicle growth status

Nixon

Ca²,

Wildermoth³

et al. 2002

Journal of Endocrinology

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Seasonal patterns of hair growth are governed, at least in part, by levels of prolactin in circulation, and although receptors for prolactin (PRLR) have been demonstrated in hair follicles, little is known of their regulation in relation to follicular cycles. In this study, a photoperiod-generated increase in prolactin was used to induce a wool follicle cycle during which changes in PRLR expression in sheep skin were determined by ribonuclease protection assay and in situ hybridisation. mRNA for prolactin and both isoforms of PRLR were also detected in skin by reverse transcription and polymerase chain reaction. As circulating prolactin began to rise from low levels, PRLR mRNA in the skin initially fell. These changes immediately preceded the catagen (regressive) phase of the hair cycle. Further increase in prolactin resulted in up-regulation of PRLR during telogen (dormancy), particularly in the epithelial hair germ, to reach a peak during proanagen (reactivation). In anagen (when follicle growth was fully re-established), PRLR mRNA returned to levels similar to those observed before the induced cycle. Hence, this longer term rise and fall of PRLR expression followed that of plasma prolactin concentration with a lag of 12-14 days. PRLR mRNA was most abundant in the dermal papilla, outer root sheath, hair germ, skin glands and epidermis. Location of PRLR in the dermal papilla and outer root sheath indicates action of prolactin on the growth-controlling centres within wool follicles. These cycle-related patterns of PRLR expression suggest dynamic regulation of PRLR by prolactin, thereby modulating hormonal responsiveness of seasonally growing hair follicles.

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“…This feature plays an important role in the regulation of these systems by producing binding surfaces with dramatically different binding affinities to the receptor. 35 Such PRL-R are expressed by human epidermal keratinocytes in vitro 36 ; in the dermal papilla, matrix, outer root sheath, lower regions of the inner root sheath, and connective tissue sheath in wool follicles of sheep 37,38 ; and in the outer root sheath of anagen HFs of mice. 22,23 This expression pattern suggests that PRL can directly alter skin and HF functions by targeting cognate, locally expressed receptors.…”

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confidence: 99%

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

Foitzik

Krause

Conrad

et al. 2006

The American Journal of Pathology

133

171

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The prototypic pituitary hormone prolactin (PRL) exerts a wide variety of bioregulatory effects in mammals and is also found in extrapituitary sites, including murine skin. Here, we show by reverse transcriptase-polymerase chain reaction and immunohistology that, contrary to a previous report, human skin and normal human scalp hair follicles (HFs), in particular, express both PRL and PRL receptors (PRL-R) at the mRNA and protein level. PRL and PRL-R immunoreactivity can be detected in the epithelium of human anagen VI HFs, while the HF mesenchyme is negative. During the HF transformation from growth (anagen) to apoptosisdriven regression (catagen), PRL and PRL-R immunoreactivity appear up-regulated. Treatment of organ-cultured human scalp HFs with high-dose PRL (400 ng/ml) results in a significant inhibition of hair shaft elongation and premature catagen development, along with reduced proliferation and increased apoptosis of hair bulb keratinocytes (Ki-67/terminal dUTP nick-end labeling immunohistomorphometry). This shows that PRL receptors, expressed in HFs, are functional and that human skin and human scalp HFs are both direct targets and sources of PRL. Our data suggest that PRL acts as an autocrine hair growth modulator with catagenpromoting functions and that the hair growth-inhibitory effects of PRL demonstrated here may underlie the as yet ill-understood hair loss in patients with hyperprolactinemia.

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Localisation of receptors for prolactin in ovine skin

Cited by 23 publications

References 24 publications

Prolactin and Its Receptor Are Expressed in Murine Hair Follicle Epithelium, Show Hair Cycle-Dependent Expression, and Induce Catagen

Prolactin and Its Receptor Are Expressed in Murine Hair Follicle Epithelium, Show Hair Cycle-Dependent Expression, and Induce Catagen

Regulation of prolactin receptor expression in ovine skin in relation to circulating prolactin and wool follicle growth status

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

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