Nell'abstract giapponese avevo letto che le sperimentazioni erano state fatte con la sola l'adenosina. Posso comunque riformulare la Domanda al Marliani, ma trovo difficile che questi, potendo, non abbia corretto da subito il tiro: che gli sarebbe costato aggiungere alla risposta che l'ATP avesse, al contrario dell'adenosina, un'efficacia terapeutica?
Il librone lo puoi linkare anche qui, come preferisci, non ti so dire se riuscirò a leggerlo nel breve periodo - ultimamente sono sommerso dagli impegni, stimolanti peraltro! - ma se è interessante come dici senz'altro lo leggerò -
Per il momento ti volevo porre all’attenzione questi articoli che sembrano interessanti e riguardano dei processi biologici non legati al controllo steorideo né alla sfera glucidico metabolica del capillizio.
Chissà che non vi siano delle possibilità terapeutiche ancora inesplorate…
Citazione:
Exp Dermatol. 1999 Aug;8(4):274-81.
Related Articles, Links
Hair growth-modulation by adrenergic drugs.
Peters EM, Maurer M, Botchkarev VA, Gordon DS, Paus R.
Department of Dermatology, Charite, Humboldt-Universitat zu Berlin, Germany.
Since we have recently shown that the beta 2-adrenoreceptor (beta 2-AR) expression of selected regions of the hair follicle (HF) epithelium as well as the number of adrenergic nerve fibers in murine skin change in a hair cycle-dependent manner, this has raised the possibility that adrenergic nerves may exert trophic functions during HF cycling. To further explore this concept, we have investigated the effect of neuro-pharmacological manipulations on hair growth (anagen) induction in quiescent telogen mouse skin in vivo. Here, we demonstrate that subcutaneous injections of the noradrenaline (NA)-depleting agent guanethidine, or of the neurotoxin 6-hydroxydopamine, but not of the beta 2-AR agonist isoproterenol induce a premature onset of anagen in the lower back skin of C57BL/6 mice. On day 20 after the start of treatment, more than 80% of the guanethidine-treated mice and ca. 65% of the 6-hydroxydopamine-treated (6-OHDA) mice exhibited premature skin darkening and hair growth at the site of drug application, whereas less than one-third of all control animals showed macroscopic signs of anagen development. This was confirmed by histology, demonstrating mature anagen VI HFs only at the immediate site of treatment with guanethidine or 6-OHDA as opposed to resting telogen HFs in the neighboring untreated skin area. This observation further supports the concept that sympathetic nerves are intimately involved in hair growth control and invites one to explore the neuro-pharmacological manipulation of piloneural interactions as a novel therapeutic strategy for the management of hair growth disorders.
Citazione:
Epithelial growth control by neurotrophins: leads and lessons from the hair follicle.
Botchkarev VA, Botchkareva NV, Peters EM, Paus R.
Department of Dermatology, Boston University School of Medicine, Boston, MA, USA.
Neurotrophins (NTs) exert many growth-regulatory functions beyond the nervous system. For example, murine hair follicles (HF) show developmentally and spatio-temporally stringently controlled expression of NTs, including nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), and NT-4, and their cognate receptors, tyrosine kinase A-C (TrkA-C) and p75 neurotrophin receptor (p75NTR). Follicular NT and NT receptor expression exhibit significant, hair cycle-dependent fluctuations on the gene and protein level, which are mirrored by changes in nerve fiber density and neurotransmitter/neuropeptide content in the perifollicular neural networks. NT-3/TrkC and NGF/TrkA signaling stimulate HF development, while NT-3, NT-4 and BDNF inhibit the growth (anagen) of mature HF by the induction of apoptosis-driven HF regression (catagen). p75NTR stimulation inhibits HF development and stimulates catagen. Since the HF is thus both a prominent target and key peripheral source of NT, dissecting the role of NTs in the control of HF morphogenesis and cyclic remodeling provides a uniquely accessible, and easily manipulated, clinically relevant experimental model, which has many lessons to teach. Given that our most recent data also implicate NTs in human hair growth control, selective NT receptor agonists and antagonists may become innovative therapeutic tools for the management of hair growth disorders (alopecia, effluvium, hirsutism). Since, however, the same NT receptor agonists that inhibit hair growth (e.g., BDNF, NT-4) can actually stimulate epidermal keratinocyte proliferation, NT may exert differential effects on defined keratinocyte subpopulations. The studies reviewed here provide new clues to understanding the complex roles of NT in epithelial tissue biology and remodeling in vivo, and invite new applications for synthetic NT receptor ligands for the treatment of epithelial growth disorders, exploiting the HF as a lead model.
Publication Types:
• Review
Hair cycle-dependent changes in adrenergic skin innervation, and hair growth modulation by adrenergic drugs.
Citazione:
Botchkarev VA, Peters EM, Botchkareva NV, Maurer M, Paus R.
Department of Dermatology, Charite, Humboldt University, Berlin, Germany.
Skin nerves may exert trophic functions during hair follicle development, growth, and/or cycling. Here, we demonstrate hair cycle-related plasticity in the sympathetic innervation of skin and hair follicle in C57BL/6 mice. Compared with telogen skin, the number of nerve fibers containing norepinephrine or immunoreactive for tyrosine hydroxylase increased during the early growth phase of the hair cycle (anagen) in dermis and subcutis. The number of these fibers declined again during late anagen. beta2-adrenoreceptor-positive keratinocytes were transiently detectable in the noncycling hair follicle epithelium, especially in the isthmus and bulge region, but only during early anagen. In early anagen skin organ culture, the beta2-adrenoreceptor agonist isoproterenol promoted hair cycle progression from anagen III to anagen IV. The observed hair cycle-dependent changes in adrenergic skin innervation on the one hand, and hair growth modulation by isoproterenol, accompanied by changes in beta2-adrenoreceptor expression of selected regions of the hair follicle epithelium on the other, further support the concept that bi-directional interactions between the hair follicle and its innervation play a part in hair growth control. This invites one to systematically explore the neuropharmacologic manipulation of follicular neuroepithelial interactions as a novel therapeutic strategy for managing hair growth disorders.
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