Electron paramagnetic resonance (EPR) spectroscopy for investigating murine telogen skin after spontaneous or depilation-induced hair growth

Depilation has greatly promoted our understanding of hair follicle biology, however, only marginally of telogen (the “resting” stage of the hair cycle). Since electron paramagnetic resonance (EPR) spectroscopy provides an instructive technique for analyzing hair biology, it may be useful for telogen research. To identify differences in murine telogen skin after a spontaneous and depilation-induced hair follicle cycling, and to analyze applicability of EPR to investigate telogen. Spontaneous or depilation-induced hair cycling in C57BL/6 mice. EPR spectroscopy of unshaven skin and of shaved hair shafts, microscopical examination of plucked or shed hair shafts, standardized histomorphometry. Melanin EPR signals did not differ qualitatively between the two examined types of skin, nor did depilation change the hair length. However, unmanipulated telogen skin revealed greater thickness, stronger EPR signals, 25% more hair shafts, and lower melanin content of individual hair shafts, as creating a much more intricate mosaic of telogen hair follicles with various numbers of hair shafts (0–3) than the skin after depilation-induced hair growth. In both types of skin empty pilary canals were found. Both groups of animals lost hair shafts which were typical of exogen (the actively controlled process of hair shedding). EPR spectroscopy can be profitably employed to study telogen. Murine telogen skin reveals a kenogen-like phenomenon (the “lag” phase following telogen and exogen when hair follicles remain empty, i.e. are devoid of hair shafts). Murine skin thickness in telogen and individual hair shaft pigmentation depend on the way of hair growth induction. Telogens after a spontaneous or depilation-induced hair growth are biologically distinct

Splenic eumelanin differs from hair eumelanin in C57BL/6 mice �

The presence of melanin in spleens of black C57BL/6 mice has been known for long. Although its origin and biological functions are still obscure, the relation of splenic melanin to the hair follicle and skin pigmentation was suggested. Here, we demonstrated using for the first time electron paramagnetic resonance spectroscopy that black-spo�ed C57BL/6 spleens contain eumelanin. Its presence here is a “yes or no ” phenomenon, as even in the groups which revealed the highest percentage of spots single organs completely devoid of the pigment were found. Percentage of the spo�ed spleens decreased, however, with the progress of telogen a�er spontaneouslyinduced hair growth. The paramagnetic properties of the spleen eumelanin differed from the hair sha � or anagen VI skin melanin. The splenic melanin revealed narrower signal, and its microwave power saturability betrayed more heterogenous population of paramagnetic centres than in the skin or hair sha � pigment. Interestingly, the pigment of dry hair sha�s and of the wet tissue of depilated anagen VI skin revealed almost identical properties. The properties of splenic melanin be�er resembled the synthetic dopa melanin (water suspension, and to a lesser degree – powder sample) than the skin/hair melanin. All these findings may indicate a limited degradation of splenic melanin as compared to the skin/hair pigment. The splenic eumelanin may at least in part originate from the skin melanin phagocyted in catagen by the Langerhans cells or macrophages and transported to the organ

How UV Light Touches the Brain and Endocrine System Through Skin, and Why

The skin, a self-regulating protective barrier organ, is empowered with sensory and computing capabilities to counteract the environmental stressors to maintain and restore disrupted cutaneous homeostasis. These complex functions are coordinated by a cutaneous neuro-endocrine system that also communicates in a bidirectional fashion with the central nervous, endocrine, and immune systems, all acting in concert to control body homeostasis. Although UV energy has played an important role in the origin and evolution of life, UV absorption by the skin not only triggers mechanisms that defend skin integrity and regulate global homeostasis but also induces skin pathology ( e.g., cancer, aging, autoimmune responses). These effects are secondary to the transduction of UV electromagnetic energy into chemical, hormonal, and neural signals, defined by the nature of the chromophores and tissue compartments receiving specific UV wavelength. UV radiation can upregulate local neuroendocrine axes, with UVB being markedly more efficient than UVA. The locally induced cytokines, corticotropin-releasing hormone, urocortins, proopiomelanocortin-peptides, enkephalins, or others can be released into circulation to exert systemic effects, including activation of the central hypothalamic-pituitary-adrenal axis, opioidogenic effects, and immunosuppression, independent of vitamin D synthesis. Similar effects are seen after exposure of the eyes and skin to UV, through which UVB activates hypothalamic paraventricular and arcuate nuclei and exerts very rapid stimulatory effects on the brain. Thus, UV touches the brain and central neuroendocrine system to reset body homeostasis. This invites multiple therapeutic applications of UV radiation, for example, in the management of autoimmune and mood disorders, addiction, and obesity. UV energy triggers skin-protective responses against stress, coordinated by the cutaneous-neuroendocrine system, and activates central neuroendocrine system pathways that regulate global homeostasis

Hair follicle pigmentation

Hair shaft melanin components (eu- or/and pheomelanin) are a long-lived record of precise interactions in the hair follicle pigmentary unit, e.g., between follicular melanocytes, keratinocytes, and dermal papilla fibroblasts. Follicular melanogenesis (FM) involves sequentially the melanogenic activity of follicular melanocytes, the transfer of melanin granules into cortical and medulla keratinocytes, and the formation of pigmented hair shafts. This activity is in turn regulated by an array of enzymes, structural and regulatory proteins, transporters, and receptors and their ligands, acting on the developmental stages, cellular, and hair follicle levels. FM is stringently coupled to the anagen stage of the hair cycle, being switched-off in catagen to remain absent through telogen. At the organ level FM is precisely coupled to the life cycle of melanocytes with changes in their compartmental distribution and accelerated melanoblast/melanocyte differentiation with enhanced secretory activity. The melanocyte compartments in the upper hair follicle also provides a reservoir for the repigmentation of epidermis and, for the cyclic formation of new anagen hair bulbs. Melanin synthesis and pigment transfer to bulb keratinocytes are dependent on the availability of melanin precursors, and regulation by signal transduction pathways intrinsic to skin and hair follicle, which are both receptor dependent and independent, act through auto-, para- or intracrine mechanisms and can be modified by hormonal signals. The important regulators are MC1 receptor its and adrenocorticotropic hormone, melanocyte stimulating hormone, agouti protein ligands (in rodents), c-Kit, and the endothelin receptors with their ligands. Melanin itself has a wide range of bioactivities that extend far beyond its determination of hair color