Duchenne muscular dystrophy (DMD) is the commonest muscular dystrophy caused by the absence of dystrophin. Stem cell therapy in DMD is one of the promising approaches for treatment. Multipotent stem cells residing in the hair follicle papilla are highly plastic. We showed that dermal papilla cells (DPC) undergo myogenic differentiation when co-cultured with different types of myoblasts including dystrophic human myoblasts. DPC incorporated into myotubes and upregulated the muscle marker, myogenin, in the co-culture with human myoblasts. DPC incorporation efficiency was low (< 5%) in all co-cultures and differed significantly (p value ≤ 0.001) between various types of myoblasts; however, no significant difference was observed between normal and dystrophic human myoblasts (p value ≤ 0.001). These encouraging findings suggested that the altered properties of dystrophic human myoblasts did not compromise the myogenic differentiation of DPC in vitro, supporting their in vivo application and possible therapeutic potential. The in vitro effects of galectin-1 and activation of Shh signaling pathway via recombinant Shh (rShh) and purmorphamine, on the myogenic differentiation of DPC, was also evaluated. None of the treatments increased myogenin expression in DPC; but, triggering Shh signaling produced a dose dependent pattern whereby the lower levels of signaling promoted myogenic differentiation while the higher levels inhibited it. Activating Shh signaling upstream of Smo, via purmorphamine, induced a biphasic differentiative response; however, the application of rShh hindered the differentiation of both cell types. Thus, murine DPC are a readily accessible source of stem cells that can undergo myogenic differentiation in vitro and their myogenic differentiation can be enhanced with proper treatment .

Inconsistent with the view that epidermal stem cells reside randomly spread along the basal layer of the epidermal rete ridges, we found that epidermal cells expressing stem cell markers in nonglabrous skin exist in direct connection with the distal end of the arrector pili muscle. The epidermal cells that express stem cell markers consist of a subpopulation of basal keratinocytes located in a niche at the lowermost portion of the rete ridges at the distal arrector pili muscle attachment site. Keratinocytes in the epidermal stem cell niche express K15, MCSP, and α6 integrin. α5 integrin marks the distal end of the APM colocalized with basal keratinocytes expressing stem cell markers located in a well-protected and nourished environment at the lowermost point of the epidermis; these cells are hypothesized to participate directly in epidermal renewal and homeostasis and also indirectly in wound healing through communication with the hair follicle bulge epithelial stem cell population through the APM. Our findings, plus a reevaluation of the literature, support the hierarchical model of interfollicular epidermal stem cell units of Fitzpatrick. This new view provides insights into epidermal control and the possible involvement of epidermal stem cells in nonmelanoma skin carcinogenesis.

Androgenic alopecia (AGA) is the most common hair loss condition in men and women. Hair loss is caused by follicle miniaturization, which is largely irreversible beyond a certain degree of follicular regression. In contrast, hair loss in telogen effluvium (TE) is readily reversible. The arrector pili muscle (APM) connects the follicle to the surrounding skin.

Background: Hair follicle miniaturization is the hallmark of male pattern hair loss (MPHL), female pattern hair loss (FPHL), and alopecia areata (AA). AA has the potential for complete hair regrowth and reversal of miniaturization. MPHL and FPHL are either irreversible or show only partial regrowth and minimal reversal of miniaturization. Hypothesis: The arrector pili muscle (APM) attachment to the hair follicle bulge, a recognized repository of stem cells may be necessary for reversal of hair follicle miniaturization. Materials and Methods: Sequential histological sections from MPHL, FPHL, AA, and telogen effluvium were used to create three-dimensional images to compare the relationship between the APM and bulge. Results: In AA, contact was maintained between the APM and the bulge of miniaturized follicles while in MPHL and FPHL contact was lost. Discussion: Contact between the APM and the bulge in AA may be required for reversal of hair follicle miniaturization. Maintenance of contact between miniaturized follicles in AA could explain the complete hair regrowth while loss of contact between the APM and the bulge in MPHL and FPHL may explain why the hair loss is largely irreversible. This loss of contact may reflect changes in stem cell biology that also underlie irreversible miniaturization.

BACKGROUND:Monilethrix is a congenital hair shaft disorder with associated fragility. Many of the changes seen in monilethrix hair on light microscopy and scanning electron microscopy are also seen in hair weathering and cosmetic damage to hair.OBJECTIVES:We used monilethrix as a model to investigate the relationship between hair protein structure and hair strength and resistance to cosmetic insult.METHODS:We applied proteomic techniques to identify novel peptide damage markers for chemical oxidative damage to hair.RESULTS:The findings suggest that specific sites in the protein structure of hair are targeted during oxidative damage from bleaching, a unique insight into how chemical damage compromises the structural integrity of the hair shaft at the molecular level.CONCLUSIONS:Applying proteomics to the study of congenital and acquired hair shaft disorders can deliver new insights into hair damage and novel strategies to strengthen hair.

Androgenetic alopecia affects both men and women. In men it produces male pattern hair loss with bitemporal recession and vertex baldness. In women it produces female pattern hair loss (FPHL) with diffuse alopecia over the mid-frontal scalp. FPHL occurs as a result of nonuniform hair follicle miniaturization within follicular units. Diffuse alopecia is produced by a reduction in the number of terminal fibres per follicular unit. Baldness occurs only when all hairs within the follicular units are miniaturized and is a relatively late event in women. The concepts of follicular units and primary and secondary hair follicles within follicular units are well established in comparative mammalian studies, particularly in sheep. However, discovery of these structures in the human scalp hair and investigation of the changes in follicular unit anatomy during the development of androgenetic alopecia have provided a clearer understanding of the early stages of androgenetic alopecia and how the male and female patterns of hair loss are related. FPHL is the most common cause of alopecia in women and approximately one-third of adult caucasian women experience hair loss. The impact of FPHL is predominantly psychological. While men anticipate age-related hair loss, hair loss in women is usually unexpected and unwelcome at any age. Treatment options to arrest hair loss progression and stimulate partial hair regrowth for FPHL include the androgen receptor antagonists spironolactone and cyproterone acetate, the 5α-reductase inhibitor finasteride and the androgen-independent hair growth stimulator minoxidil. These treatments appear to work best when initiated early. Hair transplantation should be considered in advanced FPHL that is resistant to medical treatments. Hair transplantation requires well-preserved hair growth over the occipital donor area. The psychological impact of FPHL may also be reduced by cosmetic products that improve the appearance of the hair. These agents work to minimize hair fibre breakage, improve hair volume or conceal visible bald scalp.

AIMS:To investigate the location of keratin-associated proteins (KAPs) in developing hair fiber cuticle cells using transmission electron microscopy with immunogold techniques and specific antibodies. Other studies were aimed at detecting the presence of cornified envelope proteins including involucrin and loricrin. MATEIALS AND METHODS: Polyclonal antibodies were produced in rabbits against peptides from KAPS 5.1, KAPS 10.1 ultra high-sulfur proteins.RESULTS:The KAP proteins were found to form part of the developing exocuticle and a- layer. Cornified envelope proteins (involucrin and loricrin) were absent consistent with recent findings.CONCLUSIONS:The results have been discussed in terms of a revised model for fiber cuticle surface barriers including their role in fiber cuticle surface function.