p75 Neurotrophin Receptor-Mediated Signaling Promotes Human Hair Follicle Regression (Catagen)

Peters, Eva M.J.; Stieglitz, Marit G.; Liezman, Christiane; Overall, Rupert W.; Nakamura, Motonobu; Hagen, Edward H.; Klapp, Burghard F.; Arck, Petra C.; Paus, Ralf

doi:10.2353/ajpath.2006.050163

Cited by 62 publications

(54 citation statements)

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“…As reported previously, 9,11,17,19,23 K15 (bulge marker), CD200 (bulge marker), CD34, and CD271 were strongly and differentially expressed in the outermost layer of the ORS in cells that adhered to the basement membrane ('basal cells'; Figure 1a). Other cytokeratins (K1 and K14) and integrins Figure 1 Biomarker expression profiles in human epidermis and the anagen hair follicle.…”

Section: Differential Expression Of K15 Cd200 Cd34 and Cd271mentioning

confidence: 58%

“…15 In humans, however, anti-CD34 antibodies failed to label the bulge, but instead labeled the proximal (lower) half of the ORS. 16,17 A recent study confirmed that CD271 (p75-neurotropin receptor), known as a marker of neural stem cells or neural crest cells, 18 was also expressed in the human proximal ORS; 19 thus its expression pattern resembled that of CD34.…”

mentioning

confidence: 61%

“…17,23 Recent reports suggested that CD34 and CD271 were expressed in human hair follicles, especially in the ORS proximal to the attachment site of the APM. 16,17,19 Our immunohistological assays demonstrated a similar staining pattern; however, we report for the first time that CD271 was expressed proximal to CD34. CD29 and CD49f, which are expressed around the bulge in rodents, were widely expressed in human hair follicles, and could not be used as a specific marker for the bulge in humans.…”

Section: Discussionmentioning

confidence: 83%

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Differential expression of stem-cell-associated markers in human hair follicle epithelial cells

Inoue

Aoi

Sato³

et al. 2009

Laboratory Investigation

129

118

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Several putative biomarkers have been suggested for identifying murine follicular stem cells; however, human hair follicles have a different pattern of biomarker expression, and follicular stem cell isolation methods have not been established. To isolate a stem cell population applicable to clinical settings, we conducted a comprehensive survey of the expression of stem-cell-associated (K15, CD200, CD34, and CD271) and other biomarkers (K1, K14, CD29, and CD49f) in immunohistological sections of the human epidermis and follicular outer root sheath (ORS). We also examined freshly isolated and cultured epidermal or follicular cells with single-and multicolor flow cytometry or immunocytochemistry. After sorting cells by CD200, CD34, and forward scatter (FSC) values (cell size), colony-forming assays were performed. We found that biomarkers were differentially expressed in the epidermis and ORS. Basal bulge cells were mainly K15 þ CD200 þ CD34 À CD271 À , and suprabasal cells were K15 À CD200 þ CD34 À CD271 À . We categorized follicular cells into nine subpopulations according to biomarker expression profiles. The CD200 þ CD34 À bulge cells had much higher colony-forming abilities than the CD34 þ population, and were divided into two subpopulations: a CD200 þ CD34 À FSC high (K15-rich, basal) and a CD200 þ CD34 -FSC low (K15-poor, suprabasal) population. The former formed fewer but larger-sized colonies than the latter. Follicular epithelial cell cultivation resulted in loss of K15, CD200, CD34, and CD271 expression, but maintenance of K14, CD29, and CD49f expression. We found that the bulge contained two populations with different localizations, cell sizes, and colony-forming abilities. We showed that K15, CD200, CD34, and CD271 were useful biomarkers for characterizing freshly isolated human follicular epithelial cells in diverse stages of differentiation.

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Section: Differential Expression Of K15 Cd200 Cd34 and Cd271mentioning

confidence: 58%

mentioning

confidence: 61%

Section: Discussionmentioning

confidence: 83%

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Differential expression of stem-cell-associated markers in human hair follicle epithelial cells

Inoue

Aoi

Sato³

et al. 2009

Laboratory Investigation

129

118

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“…Hair cycle morphology and development may be regulated by NGF as well as neurotrophins (4,93,94,96,98,620,638). In mice, the p75 neurotrophin receptor has been shown to control apoptosis-driven hair follicle regression.…”

Section: B Ngf and Nt Receptorsmentioning

confidence: 99%

Neuronal Control of Skin Function: The Skin as a Neuroimmunoendocrine Organ

Roosterman¹,

Goerge

Schneider

et al. 2006

Physiological Reviews

556

521

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This review focuses on the role of the peripheral nervous system in cutaneous biology and disease. During the last few years, a modern concept of an interactive network between cutaneous nerves, the neuroendocrine axis, and the immune system has been established. We learned that neurocutaneous interactions influence a variety of physiological and pathophysiological functions, including cell growth, immunity, inflammation, pruritus, and wound healing. This interaction is mediated by primary afferent as well as autonomic nerves, which release neuromediators and activate specific receptors on many target cells in the skin. A dense network of sensory nerves releases neuropeptides, thereby modulating inflammation, cell growth, and the immune responses in the skin. Neurotrophic factors, in addition to regulating nerve growth, participate in many properties of skin function. The skin expresses a variety of neurohormone receptors coupled to heterotrimeric G proteins that are tightly involved in skin homeostasis and inflammation. This neurohormone-receptor interaction is modulated by endopeptidases, which are able to terminate neuropeptide-induced inflammatory or immune responses. Neuronal proteinase-activated receptors or transient receptor potential ion channels are recently described receptors that may have been important in regulating neurogenic inflammation, pain, and pruritus. Together, a close multidirectional interaction between neuromediators, high-affinity receptors, and regulatory proteases is critically involved to maintain tissue integrity and regulate inflammatory responses in the skin. A deeper understanding of cutaneous neuroimmunoendocrinology may help to develop new strategies for the treatment of several skin diseases.

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“…HF immune privilege, connective tissue sheath (CTS) mast cell degranulation. (see Arck et al, 2005a; Bodó et al, 2005 and2007; Botchkarev et al, 2004; Colombe et al., 2007; Deplewski and Rosenfield, 2000;Hasse et al, 2007; Kauser et al, 2006;Ohnemus et al, 2006;Paus et al, 2006;Peters et al, 2006b and2007;Philp et al, 2004;Slominski et al, 2007;Telek et al, 2007;Zouboulis et al, 2007) While this remains to be conclusively demonstrated, it is likely that HFeSC are fully integrated into this neuroendocrine tapestry of general HF biology. However, all we have to go by currently are some pointers to potentially important elements in the as yet obscure neuroendocrinology of HFeSC.…”

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confidence: 99%

(Neuro-)endocrinology of epithelial hair follicle stem cells

Paus

Arck

Tiede

2008

Molecular and Cellular Endocrinology

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The hair follicle is a repository of different types of somatic stem cells. However, even though the hair follicle is both a prominent target organ and a potent, non-classical site of production and/or metabolism of numerous polypetide-and steroid hormones, neuropeptides, neurotransmitters and neurotrophins, the (neuro-) endocrine controls of hair follicle epithelial stem cell (HFeSC) biology remain to be systematically explored.Focussing on HFeSCs, we attempt here to offer a "roadmap through terra incognita" by listing key open questions, by exploring endocrinologically relevant HFeSC gene profiling and mouse genomics data, and by sketching several clinically relevant pathways via which systemic and/or locally generated (neuro-)endocrine signals might impact on HFeSC. Exemplarily, we discuss e.g. the potential roles of glucocorticoid and vitamin D receptors, the hairless gene product, thymic hormones, bone morphogenic proteins (BMPs) and their antagonists, and Skg-3 in HFeSC biology. Furthermore, we elaborate on the potential role of nerve growth factor (NGF) and substance P-dependent neurogenic inflammation in HFeSC damage, and explore how neuroendocrine signals may influence the balance between maintenance and destruction of hair follicle immune privilege, which protects these stem cells and their progeny. These considerations call for a concerted research effort to dissect the (neuro)-endocrinology of HFeSCs much more systematically than before. The hair follicle (HF) and its special, associated mesenchyme (i.e. the connective tissue sheath, CTS) are repositories of different types of somatic stem cells (epithelial, mesenchymal, neural, mesenchymal) (Cotsarelis, 2006; Kruse et al., 2006;Millar, 2005;Ohyama et al., 2006;Tiede et al. 2007;Waters et al., 2007;Yu et al., 2006). These HFassociated stem cell populations are critical for HF development and function, including HF pigmentation (Nishimura et al., 2002(Nishimura et al., , 2005Sarin and Artandi, 2007). Fig. 1 shows several important, recognized hair follicle-associated stem cell populations and their bestcharacterized location(s) in the pilosebaceous unit, though it must be kept in mind that the indicated ones are unlikely to be the only stem cell population associated with mammalian skin appendages (Tiede et al. 2007). Clinical importance of hair follicle stem cellsHair follicle epithelial stem cells (HFeSCs) are clinically important, since they can be key targets for pathological processes, such as an autoaggressive inflammatory cell attack on HFeSC, e.g. in lupus erythematosus or lichen planopilaris, where the destruction of bulge HFeSCs (see Fig.1) abolishes the hair follicle's capacity to cycle and to rhythmically regenerate itself, leading to scarring alopecia (Cotsarelis, 2006;Hiroi et al., 2006;Mobini et al., 2005;Paus, 2006). Likewise, a gradual loss of HF melanocyte stem cells may exhaust the HF pigmentary unit's capacity to generate itself and to produce melanin and thus likely plays a key role in hair graying (Commo et al., 2004;...

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p75 Neurotrophin Receptor-Mediated Signaling Promotes Human Hair Follicle Regression (Catagen)

Cited by 62 publications

References 44 publications

Differential expression of stem-cell-associated markers in human hair follicle epithelial cells

Differential expression of stem-cell-associated markers in human hair follicle epithelial cells

Neuronal Control of Skin Function: The Skin as a Neuroimmunoendocrine Organ

(Neuro-)endocrinology of epithelial hair follicle stem cells

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