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Selective photothermolysis to target sebaceous glands: Theoretical estimation of parameters and preliminary results using a free electron laser.
Sakamoto FH, et al
BACKGROUND AND OBJECTIVES:
The success of permanent laser hair removal suggests that selective photothermolysis (SP) of sebaceous glands, another part of hair follicles, may also have merit. About 30% of sebum consists of fats with copious CH(2) bond content. SP was studied in vitro, using free electron laser (FEL) pulses at an infrared CH(2) vibrational absorption wavelength band.
Absorption spectra of natural and artificially prepared sebum were measured from 200 to 3,000 nm, to determine wavelengths potentially able to target sebaceous glands. The Jefferson National Accelerator superconducting FEL was used to measure photothermal excitation of aqueous gels, artificial sebum, pig skin, human scalp, and forehead skin (sebaceous sites). In vitro skin samples were exposed to FEL pulses from 1,620 to 1,720 nm, spot diameter 7-9.5 mm with exposure through a cold 4°C sapphire window in contact with the skin. Exposed and control tissue samples were stained using H&E, and nitroblue tetrazolium chloride staining (NBTC) was used to detect thermal denaturation.
Natural and artificial sebum both had absorption peaks near 1,210, 1,728, 1,760, 2,306 and 2,346 nm. Laser-induced heating of artificial sebum was approximately twice that of water at 1,710 and 1,720 nm, and about 1.5× higher in human sebaceous glands than in water. Thermal camera imaging showed transient focal heating near sebaceous hair follicles. Histologically, skin samples exposed to ∼1,700 nm, ∼100-125 milliseconds pulses showed evidence of selective thermal damage to sebaceous glands. Sebaceous glands were positive for NBTC staining, without evidence of selective loss in samples exposed to the laser. Epidermis was undamaged in all samples.
SP of sebaceous glands appears to be feasible. Potentially, optical pulses at ∼1,720 or ∼1,210 nm delivered with large beam diameter and appropriate skin cooling in approximately 0.1 seconds may provide an alternative treatment for acne. Lasers Surg. Med. © 2011 Wiley Periodicals, Inc.
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Dermatol Online J. 2010;16:3.
Does D matter? The role of vitamin D in hair disorders and hair follicle cycling.
Amor KT, Rashid RM, Mirmirani P.
"...Limited studies have been done in humans to elaborate the role of vitamin D in the hair cycle. A potential application for vitamin D is in chemotherapy-induced hair loss. Topical calcitriol has been shown to protect against chemotherapy-induced alopecia caused by paclitaxel and cyclophosphamide. However, topical calcitriol failed to protect against chemotherapy-induced hair loss caused by a combination of 5-fluorouracil, doxorubicin, and cyclophosphamide and a combination of cyclophosphamide, methotrexate, and 5-fluorouracil [36, 37]. The ability of topical calcitriol to prevent chemotherapy-induced hair loss may therefore depend on the chemotherapy agents used. Of note, the studies in which no effects were observed, were small and may have used doses of vitamin D that were inadequate to protect against chemotherapy-induced hair loss. The more potent vitamin D3 analogs used on mice by Vegesna et al. have yet to be evaluated in humans.....
It has been suggested that an optimal concentration of vitamin D is necessary to delay the aging phenomena, including hair loss. A cross sectional study of 296 healthy men was done to determine the association, if any, between male pattern baldness and serum 25-hydroxyvitamin D levels. Based on this study, the extent and severity of male pattern baldness does not appear to be associated with serum 25-hydroxyvitamin D levels . Additional studies in subjects with age-related or senescent hair thinning as well as in women with female pattern hair loss could be considered to see if there is an association of hair loss with serum 25-hydroxyvitamin D levels.
Because it is known that the absence of VDR leads to hair loss, it was hypothesized that there may be VDR gene polymorphisms (Bsml, Apal, and Taql) in patients with alopecia areata. A study of VDR genotypes in 32 patients with alopecia areata and 27 controls showed no association between these VDR gene polymorphisms and alopecia areata. A separate study also showed that there was no relationship between the VDR gene FokI polymorphism and alopecia areata......
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The role of natural killer cells in autoimmune blistering diseases.
Zakka LR, et al
The major focus of this paper is to describe and evaluate current information on the role of natural killer cells (NK cells) in the pathogenesis of blistering diseases. Until now, only pemphigus vulgaris (PV) has been studied. One co-culture study demonstrated that CD4(+) T cells from the peripheral blood or perilesional skin of patients with active disease proliferate and secrete cytokines in the presence of major histocompatibility class II-expressing NK cells loaded with antigenic desmoglein self-peptides. Another study showed that NK cells can contribute to a T helper type 2-biased immune response through impaired interleukins (IL)-12 signaling and upregulation of IL, IL-10 and IL-5. Although significant data on other blistering diseases are unavailable at present, some studies implicate NK cells in disease progression. For instance, information on the role of NK cells in psoriasis and their production of tumor necrosis factor-á (TNF-á) will be provided since several TNF-á-inhibitors are used in its treatment. Studies on hair loss due to alopecia areata are also included in this paper because NK cells seem to play a key role in its pathogenesis. This review highlights the potential importance of NK cells and NKT cells as members of the large repertoire of cells and soluble mediators that play a critical role in pathogenesis of blistering diseases and other autoimmune diseases involving the skin. Therefore, the authors advocate a greater focus and interest on the study of the interaction of NK cells and the skin.]]>
De novo formation and ultra-structural characterization of a fiber-producing human hair follicle equivalent in vitro.
Lindner G, Horland R, Wagner I, Ata B, Lauster R.
Across many tissues and organs, the ability to create an organoid, the smallest functional unit of an organ, in vitro is the key both to tissue engineering and preclinical testing regimes. The hair follicle is an organoid that has been much studied based on its ability to grow quickly and to regenerate after trauma. But hair follicle formation in vitro has been elusive. Replacing hair loss due to pattern baldness or more severe alopecia, including that induced by chemotherapy, remains a significant unmet medical need. By carefully analyzing and recapitulating the growth conditions of hair follicle formation, we recreated human hair follicles in tissue culture that were capable of producing hair. Our microfollicles contained all relevant cell types and their structure and orientation resembled in some ways excised hair follicle specimens from human skin. This finding offers a new window onto hair follicle development. Having a robust culture system for hair follicles is an important step towards improved hair regeneration as well as to an understanding of how marketed drugs or drug candidates, including cancer chemotherapy, will affect this important organ.
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Copyright © 2003 European Molecular Biology Organization
Laminin-10 is crucial for hair morphogenesis
This study, for the first time, describes the critical role of the extracellular matrix/BMZ in skin morphogenesis. We have shown that laminin-10 is the primary laminin of elongating hair germs, and that absence of laminin-10 results in arrest of hair follicle development at the hair germ elongation phase. Interestingly, the application of exogenous laminin-10 promoted restoration of hair follicle development in Lama5 –/– skin. To our knowledge, this is the first instance of protein-mediated therapy in the correction of a cutaneous developmental defect. The method we employed, incubation of full-thickness embryonic skin in a laminin-10-containing solution, effectively resulted in the diffusion of laminin-10 into the BMZ of developing hair follicles. ....snip.. .As small amounts of laminin-11 were present in our purified laminin-10 samples, we cannot rule out the possibility that laminin-11 might also facilitate hair follicle development. However, as laminin â2-deficient mice have no hair defects (Noakes et al., 1995), and a downregulation of the laminin â2 chain was seen during mouse hair germ elongation in our studies, it is not likely that laminin-11 plays a major role in hair follicle development in the skin.Our results, as well as the results of a number previous studies, suggest that laminin-10 supports hair follicle development through a mechanism other than the maintenance of dermal–epithelial cohesion. A comparison between inhibition of laminin-5 and laminin-10 in the skin illustrates this point. In human skin xenografts, laminin-5 antibodies induced extensive epidermal detachment (Lazarova et al., 2000; M.P.Marinkovich, unpublished data) within 24 h of application, while in our studies, skin treated with laminin-10 antibodies did not show blisters or epidermal detachment even after 3 weeks. Similarly, extensive blistering is seen in patients with HJEB, who lack laminin-5. Absence of laminin-5 in Lama3 –/– mice produced extensive epidermal detachment as well as detachment-associated cell death (anoikis) (Ryan et al., 1999). In contrast, in our studies, we were unable to demonstrate significant epidermal detachment or anoikis in Lama5 –/– mouse skin. On the other hand, while inhibition of laminin-10 in both human and murine skin produced marked effects on hair follicle development, no hair follicle defects were demonstrated in laminin-5/6 null mouse skin (Ryan et al., 1999), and hair follicle development is typically normal in HJEB patients (Skoven and Drzewiecki, 1979). In conclusion, laminin-5 and laminin-10 appear to have non-overlapping functions in the skin, with laminin-5 promoting epidermal adhesion and laminin-10 promoting epithelial development.In our studies of BMZ structure in Lama5 –/– skin, lamina densa assembly was markedly abnormal, while exogenous laminin-10 corrected these defects. These results highlight the role that laminin-10 plays in lamina densa assembly in epithelial BMZs. However, the question arises as to whether BMZ assembly is necessary for hair follicle formation. For example, a number of alterations of BMZ assembly have been described in skin that do not affect hair follicle development. The absence of â4 integrin in humans produces junctional epidermolysis bullosa with pyloric atresia. In this disease, hemidesmosome formation is markedly abnormal and dermal– epidermal cohesion is severely impaired, but hair follicle abnormalities have never been reported in conjunction with this syndrome (Fine et al., 2000). Similarly, â4 integrin null mice show a similar lack of epidermal cohesion and hemidesmosome formation, but normal hair follicle development. Even the combined absence of á6â4 integrin and á3 integrin in Intá3/Intá6 –/– mice, which produced extensive impairment of lamina densa and hemidesmosome formation as well as extensive disruption of epidermal adhesion, did not significantly affect hair follicle formation. From these observations, it appears likely that neither an epithelial attachment defect nor a BMZ assembly defect can by themselves account for the lack of hair follicle development in Lama5 –/– skin.In contrast to â4 or á3 integrin deficiency, ablation of â1 integrin markedly inhibited hair follicle development. Findings in â1 integrin conditionally null skin were remarkably similar to our findings with Lama5 –/– skin, and include formation of an interrupted lamina densa and arrest of hair follicle development at the hair germ elongation stage. These previous findings correlate well with our studies of antibody-induced â1 integrin inhibition in the developing human scalp xenografts, in which â1 inhibition inhibited hair follicle development. As á3â1 integrin is a major laminin-10 receptor (Kikkawa et al., 2000), these results support a model in which laminin-10 promotes hair follicle development through â1 integrin signaling. This remains to be further studied.It appears likely that the lack of epithelial proliferative downgrowths in mutant skin grafts are the direct result of impaired Shh production and signaling evidenced by a decrease in expression of Shh and its downstream effector Gli1 in Lama5 –/– skin. Thus, it is possible that interruption of a specific signaling pathway arrested hair follicle development in Lama5 –/– mice. Shh expression and signaling are known to depend on the correct signaling of regulators such as isoforms of the BMP, WNT and TGF families of proteins, and it is possible that laminin-10 may in turn influence the localization, expression or activity of one or more of these proteins. Of note, it is interesting that the alterations of epithelial development in Lama5 –/– skin are selective, and do not affect other aspects of skin development such as epidermal differentiation or blood vessel formation.As the effects of laminin-10 appear specifically directed at the elongating hair germ, it is tempting to speculate that laminin-10 required for this process would be located in the follicular epithelial BMZ and be of keratinocyte origin. Alternatively, it has previously been suggested that a dermal signal is required for elongation of hair germs. In particular, laminin-10 is a component of dermal blood vessels, and has been shown to act as a potent substrate for â1 integrin-mediated endothelial cell signaling and migration (Doi et al., 2002). Thus, it is possible that interactions mediated by laminin-10 in blood vessels could account for dermal contributions necessary for hair germ elongation. Additional experiments are currently under way to compare the contributions of keratinocyte and blood vessel laminin-10 towards hair follicle development.It is also possible that lack of laminin-10 could impair blood vessel function. This could produce hypoxic conditions which impact on hair follicle development either in the hair regrowth cycle or embryonic skin morphogenesis. However, blood vessels were shown to form in mutant skin, and viability in both Lama5 –/– and Lama5 +/+ grafts was equivalent, approaching 100%, and with a lack of significant apoptosis in the absence of laminin-10. Therefore, hypoxia as a sole explanation for lack of hair follicle development in Lama5 –/– grafts seems unlikely. Similarly, no differences in apoptosis were seen in â1 integrin-deficient hair follicles.
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