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• W1973199617 abstract "repeated epilation postnatal day wild type The repeated epilation (Er) mouse exhibits the epidermal phenotype that is caused by a truncated mutation in the 14-3-3σ gene (stratifin, sfn) (Herron et al., 2005Herron B.J. Liddell R.A. Parker A. et al.A mutation in stratifin is responsible for the repeated epilation (Er) phenotype in mice.Nat Genet. 2005; 37: 1210-1212Crossref PubMed Scopus (59) Google Scholar; Li et al., 2005Li Q. Lu Q. Estepa G. et al.Identification of 14-3-3sigma mutation causing cutaneous abnormality in repeated-epilation mutant mouse.Proc Natl Acad Sci USA. 2005; 102: 15977-15982Crossref PubMed Scopus (56) Google Scholar). The homozygous Er/Er mice die at birth with an epidermis that is characterized by an expanding intermediate cell layer and lack of formation of the granular and cornified layers (Herron et al., 2005Herron B.J. Liddell R.A. Parker A. et al.A mutation in stratifin is responsible for the repeated epilation (Er) phenotype in mice.Nat Genet. 2005; 37: 1210-1212Crossref PubMed Scopus (59) Google Scholar; Li et al., 2005Li Q. Lu Q. Estepa G. et al.Identification of 14-3-3sigma mutation causing cutaneous abnormality in repeated-epilation mutant mouse.Proc Natl Acad Sci USA. 2005; 102: 15977-15982Crossref PubMed Scopus (56) Google Scholar). In contrast, heterozygous Er/+ mice are indistinguishable from wild-type (WT) siblings in the first 2 weeks after birth, then display repeated hair loss and regrowth (Guenet et al., 1979Guenet J.L. Salzgeber B. Tassin M.T. Repeated epilation: a genetic epidermal syndrome in mice.J Heredity. 1979; 70: 90-94PubMed Google Scholar). 14-3-3σ is known to be expressed in the stratified squamous epithelium, but its expression and function in the hair follicle remain largely unknown. In the current study, using Er/+ mice containing one allele expressing a dominant-negative 14-3-3σ mutant protein, we characterized the function of 14-3-3σ during hair follicle cycling. Hair growth undergoes cycles of three stages: the growing phase (anagen), the regression phase (catagen), and the resting phase (telogen) (Muller-Rover et al., 2001Muller-Rover S. Handjiski B. van der Veen C. et al.A comprehensive guide for the accurate classification of murine hair follicles in distinct hair cycle stages.J Invest Dermatol. 2001; 117: 3-15Crossref PubMed Google Scholar). After telogen, the club hair is eventually shed (exogen) and replaced by new hair (Stenn and Paus, 2001Stenn K.S. Paus R. Controls of hair follicle cycling.Physiol Rev. 2001; 81: 449-494Crossref PubMed Scopus (1119) Google Scholar; Milner et al., 2002Milner Y. Sudnik J. Filippi M. et al.Exogen, shedding phase of the hair growth cycle: characterization of a mouse model.J Invest Dermatol. 2002; 119: 639-644Crossref PubMed Scopus (89) Google Scholar; Higgins et al., 2009Higgins C.A. Westgate G.E. Jahoda C.A. From telogen to exogen: mechanisms underlying formation and subsequent loss of the hair club fiber.J Invest Dermatol. 2009; 129: 2100-2108Crossref PubMed Scopus (62) Google Scholar). Er/+ mice showed no gross physical abnormality at birth, but developed severe alopecia, starting around postnatal day 13 (pd13) at the end of the first anagen phase (Figure 1a) and progressing gradually. By the beginning of telogen, at ∼pd22–24, these mice had lost almost all of their hairs (Figure 1a). The hair-loss phenotype was maintained for several days until anagen started again at pd30–32 and the hairs reappeared. The Er/+ mice almost regained a pelage similar to that in WT controls by pd34 (Figure 1a). At ∼pd40, the Er/+ mice underwent a second wave of hair loss, mimicking the previous one, although this cycle exhibited a less striking appearance, as it was less synchronized (Figure 1a). To investigate whether the hair loss in Er/+ mice corresponds to changes during hair follicle cycling, we performed a histological examination. The morphogenesis and differentiation of hair follicle were not impaired in Er/+ mice (data not shown). The follicular infundibular wall was generally thicker in the Er/+ mice and more prominent when the hair follicle moved into the catagen and telogen phases (Figure 1b and data not shown). The Er/+ mice showed dilated and plugged follicular ostia (Figure 1b, indicated by arrows). Some affected follicles had a cystic appearance of the keratin-dilated infundibulum. Sebaceous glands appeared hyperplastic and contiguous with the follicular plugs (Figure 1b, indicated by arrowheads at the right). The hair growth and shape, and hair follicle cycling were not obviously affected in the Er/+ mice. Therefore, it is likely that the weakened anchorage of hair shafts causes the alopecia phenotype in Er/+ mice. To test this hypothesis, we compared the sizes of the hair clubs in Er/+ and WT mice by applying adhesive tape strips to the backs of WT and Er/+ mice at pd20 and gently pulling the hair out. In contrast to the wide club shape at the end of the normal hair (Figure 2a1 and a2), the Er/+ hair showed a smaller club, with few club sheath cells attached (Figure 2a3 and a4). The club fiber is believed to be held in place by trichilemmal keratin, which is characterized by numerous anchoring protrusions (Pinkus et al., 1981Pinkus H. Iwasaki T. Mishima Y. Outer root sheath keratinization in anagen and catagen of the mammalian hair follicle. A seventh distinct type of keratinization in the hair follicle: trichilemmal keratinization.J Anatomy. 1981; 133: 19-35PubMed Google Scholar; Higgins et al., 2009Higgins C.A. Westgate G.E. Jahoda C.A. From telogen to exogen: mechanisms underlying formation and subsequent loss of the hair club fiber.J Invest Dermatol. 2009; 129: 2100-2108Crossref PubMed Scopus (62) Google Scholar). Histological examination of Er/+ hair follicles showed that the few hairs that were still retained during the catagen and telogen phases failed to form a normal club hair structure, showing a significant reduction in anchoring protrusions in keratinized cells (Figure 2b3 vs b1 and b4 vs b2). The trichilemmal keratin of the club fiber is formed by the companion layer cells and the defect may reflect a dysfunction of the companion cells (Winter et al., 1998Winter H. Langbein L. Praetzel S. et al.A novel human type II cytokeratin, K6hf, specifically expressed in the companion layer of the hair follicle.J Invest Dermatol. 1998; 111: 955-962Crossref PubMed Scopus (122) Google Scholar; Gu and Coulombe, 2007Gu L.H. Coulombe P.A. Keratin expression provides novel insight into the morphogenesis and function of the companion layer in hair follicles.J Invest Dermatol. 2007; 127: 1061-1073Abstract Full Text Full Text PDF PubMed Scopus (30) Google Scholar). Consistent with this, we observed that 14-3-3σ was highly expressed in the sheath cells anchoring the club fiber and was associated more with keratin 6-positive companion cells and less with keratin 14-expressing outer root sheath cells in the pd17 catagen phase (Figure 2c and d). The keratin 6-positive companion layer cells were arranged in a regular elongated capsule shape in close contact with the hair fiber (Figure 2e1, indicated by an arrow). In contrast, the club pit in Er/+ hair was short and deformed, and few cells anchored to the hair fiber, although the number of keratin 6-positive companion cells in the Er/+ hair follicle were increased (Figure 2f1, indicated by an arrow). The accumulation of multiple layers of keratin 6-positive cells at the end of the pit led to crowding of the cells into a plug that seems to prevent pit elongation (Figure 2). Desmoglein 3 is the main component of the desmosome junction complex and is important for anchoring the telogen hair (Koch et al., 1998Koch P.J. Mahoney M.G. Cotsarelis G. et al.Desmoglein 3 anchors telogen hair in the follicle.J Cell Sci. 1998; 111: 2529-2537PubMed Google Scholar; Hanakawa et al., 2004Hanakawa Y. Li H. Lin C. et al.Desmogleins 1 and 3 in the companion layer anchor mouse anagen hair to the follicle.J Invest Dermatol. 2004; 123: 817-822Abstract Full Text Full Text PDF PubMed Scopus (40) Google Scholar). Desmoglein 3 was expressed in Er/+ hair sheath companion cells; however, its distribution on the margin between the anchoring cells and hair fiber appeared pitted and very different from that in normal WT club hair (Figure 2e1–e4 and f1–f4). A similar observation was obtained when we stained the developing club hair with another desmosomal junction component, plakoglobin (Figure 2g1–g4 and h1–h4). Taken together, these data showed that a normal level of 14-3-3σ was important to maintain the companion cell physiology. How 14-3-3σ mediates the differentiation and function of companion cells requires further investigation. Interestingly, Er/+ mice have alopecia phenotypes similar to those of keratin 17 (K17) null mice, and K17 binds to 14-3-3σ to regulate protein synthesis and cell growth during skin wound healing (Kim et al., 2006Kim S. Wong P. Coulombe P.A. A keratin cytoskeletal protein regulates protein synthesis and epithelial cell growth.Nature. 2006; 441: 362-365Crossref PubMed Scopus (363) Google Scholar). It raises the possibility that K17 functions in the hair follicle through the 14-3-3σ signaling pathway. Experimental animal care and use were approved by the Institutional Animal Care and Use Committee of the University of Louisville. This work was supported by grants NIH/NCRR COBRE 5 P20 RR018733 (to Q. Li), 5 P20 RR017702 (to Q. Lu), NIH R01-EY018830 (to Q. Lu), Research to Prevent Blindness, NY, and NIH EY015636." @default.
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• W1973199617 title "14-3-3σ Is Required for Club Hair Retention" @default.
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