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• W2034642769 abstract "hair follicle The hair follicle (HF) is a skin appendage that shows cyclic activity with periods of growth and hair fiber production (anagen), apoptosis-driven involution (catagen), and relative resting/hair shedding (telogen/exogen) (Stenn and Paus, 2001Stenn K.S. Paus R. Controls of hair follicle cycling.Physiol Rev. 2001; 81: 449-494Crossref PubMed Scopus (1033) Google Scholar). Proliferation, differentiation, and apoptosis in HF keratinocytes are controlled by a number of signaling molecules that belong to the bone morphogenic protein/transforming growth factor-β, epidermal growth factor, fibroblast growth factor, Hedgehog, IGF, Notch, neurotrophin, tumor necrosis factor, and Wnt families (Stenn and Paus, 2001Stenn K.S. Paus R. Controls of hair follicle cycling.Physiol Rev. 2001; 81: 449-494Crossref PubMed Scopus (1033) Google Scholar; Botchkarev and Kishimoto, 2003Botchkarev V.A. Kishimoto J. Molecular control of epithelial–mesenchymal interactions during hair follicle cycling.J Invest Dermatol Symp Proc. 2003; 8: 46-55Abstract Full Text Full Text PDF PubMed Scopus (212) Google Scholar; Paus and Foitzik, 2004Paus R. Foitzik K. In search of the “hair cycle clock”: a guided tour.Differentiation. 2004; 72: 489-511Crossref PubMed Scopus (208) Google Scholar). The decrease in proliferative activity or activation of apoptosis in the matrix region leads to hair growth retardation and/or alterations in HF cyclic activity. Therefore, molecules involved in the control of cell proliferation and/or apoptosis are of interest for hair growth modulation (Cotsarelis and Millar, 2001Cotsarelis G. Millar S.E. Towards a molecular understanding of hair loss and its treatment.Trend Mol Med. 2001; 7: 293-301Abstract Full Text Full Text PDF PubMed Scopus (196) Google Scholar). Survivin is a member of the inhibitor of apoptosis protein family, and has been implicated in the control of cell proliferation, as well as in the inhibition of apoptosis (Ambrosini et al., 1998Ambrosini G. Adida C. Sirugo G. Altieri D.C. Induction of apoptosis and inhibition of cell proliferation by survivin gene targeting.J Biol Chem. 1998; 273: 11177-11182Crossref PubMed Scopus (427) Google Scholar; Wheatley and McNeish, 2005Wheatley S.P. McNeish I.A. Survivin: a protein with dual roles in mitosis and apoptosis.Int Rev Cytol. 2005; 247: 35-88Crossref PubMed Scopus (146) Google Scholar). Survivin functions as a component of the chromosomal passenger complex, which is essential for cell division (Li et al., 1999Li F. Ackermann E.J. Bennett C.F. Rothermel A.L. Plescia J. Tognin S. et al.Pleiotropic cell-division defects and apoptosis induced by interference with survivin function.Nat Cell Biol. 1999; 1: 461-466Crossref PubMed Scopus (546) Google Scholar; Temme et al., 2003Temme A. Rieger M. Reber F. Lindemann D. Weigle B. Diestelkoetter-Bachert P. et al.Localization, dynamics, and function of survivin revealed by expression of functional survivinDsRed fusion proteins in the living cell.Mol Biol Cell. 2003; 14: 78-92Crossref PubMed Scopus (77) Google Scholar). In addition, survivin inhibits apoptosis by either directly or indirectly interfering with the functions of caspases (Tamm et al., 1998Tamm I. Wang Y. Sausville E. Scudiero D.A. Vigna N. Oltersdorf T. et al.IAP-family protein survivin inhibits caspase activity and apoptosis induced by Fas (CD95), Bax, caspases, and anticancer drugs.Cancer Res. 1998; 58: 5315-5320PubMed Google Scholar; Banks et al., 2000Banks D.P. Plescia J. Altieri D.C. Chen J. Rosenberg S.H. Zhang H. et al.Survivin does not inhibit caspase-3 activity.Blood. 2000; 96: 4002-4003Crossref PubMed Google Scholar). Transgenic mice expressing survivin under control of the keratin 14 promoter show significantly reduced number of apoptotic cells in the epidermis after UV exposure (Grossman et al., 2001Grossman D. Kim P.J. Blanc-Brude O.P. Brash D.E. Tognin S. Marchisio P.C. et al.Transgenic expression of survivin in keratinocytes counteracts UVB-induced apoptosis and cooperates with loss of p53.J Clin Invest. 2001; 108: 991-999Crossref PubMed Scopus (193) Google Scholar). In contrast, molecular survivin antagonists increase the susceptibility of numerous cell lines to apoptosis (Xia et al., 2002Xia C. Xu Z. Yuan X. Uematsu K. You L. Li K. et al.Induction of apoptosis in mesothelioma cells by antisurvivin oligonucleotides.Mol Cancer Ther. 2002; 1: 687-694PubMed Google Scholar; Kappler et al., 2004Kappler M. Bache M. Bartel F. Kotzsch M. Panian M. Wurl P. et al.Knockdown of survivin expression by small interfering RNA reduces the clonogenic survival of human sarcoma cell lines independently of p53.Cancer Gene Ther. 2004; 11: 186-193Crossref PubMed Scopus (117) Google Scholar). Survivin expression is elevated in majority of human cancers. It has potential as a marker for diagnostics, as well as a prognostic and therapeutic target for radio- and chemotherapy (Altieri, 2003Altieri D.C. Survivin in apoptosis control and cell cycle regulation in cancer.Prog Cell Cycle Res. 2003; 5: 447-452PubMed Google Scholar; Rodel et al., 2005Rodel F. Hoffmann J. Distel L. Herrmann M. Noisternig T. Papadopoulos T. et al.Survivin as a radioresistance factor, and prognostic and therapeutic target for radiotherapy in rectal cancer.Cancer Res. 2005; 65: 4881-4887Crossref PubMed Scopus (239) Google Scholar). The dual functions of survivin in promoting cell proliferation and preventing apoptosis raises a question about its involvement in regulating anagen and catagen phases of the hair cycle, during which hair matrix keratinocytes extensively proliferate and undergo apoptosis (Stenn and Paus, 2001Stenn K.S. Paus R. Controls of hair follicle cycling.Physiol Rev. 2001; 81: 449-494Crossref PubMed Scopus (1033) Google Scholar; Botchkareva et al., 2006Botchkareva N.V. Ahluwalia G. Shander D. Apoptosis in the hair follicle.J Invest Dermatol. 2006; 126: 258-264Crossref PubMed Scopus (85) Google Scholar). To explore survivin expression in human skin, survivin gene transcription and survivin protein expression in the epidermis and HFs was characterized by real-time PCR analysis and immunohistochemistry, respectively (human scalp skin was obtained from face-lifts remains with written patient consent from five different individuals; the study was approved by an independent Institutional Review Board to ensure subject protection and adherence to the Declaration of Helsinki Principles). By real-time PCR analysis, survivin mRNA expression was observed in anagen HFs, as well as in the epidermis (PCR primer set was obtained from SuperArray Bioscience Corporation, Frederick, MD). Relative quantification revealed that levels of survivin mRNA are substantially higher in the HF than in the epidermis (Figure 1a).To determine localization of survivin in skin, rabbit polyclonal antibody against human survivin protein (1:1,000; Chemicon International Inc., Temecula, CA) was applied, using 8-μm frozen tissue sections fixed in 10% formalin (10 min) and post-fixed in ethanol-acetic acid (5 min, −20°C) and the tyramide-amplification method, as described before (Botchkareva et al., 2003Botchkareva N.V. Khlgatian M. Longley B.J. Botchkarev V.A. Gilchrest B.A. SCF/c-kit signaling is required for cyclic regeneration of the hair pigmentation unit.FASEB J. 2003; 15: 645-658Crossref Scopus (187) Google Scholar). In the epidermis, survivin was expressed only in few basal cells (Figure 1b). In the anagen HF, survivin was prominently expressed in the hair matrix and outer root sheath, and survivin colocalized with proliferative marker Ki-67, as determined by using rabbit monoclonal antibody against Ki-67 (Dako, Carpinteria, CA) (Figure 1c and d). Double immunostaining with antibody against survivin and the marker of melanocytes pMel-17 (using chicken anti-gp100/pMel-17; Zymed Laboratories, San Francisco, CA) revealed that none of the cells expressing survivin either in the outer root sheath or hair matrix showed pMel-17 immunoreactivity in anagen and early-catagen HFs, suggesting that survivin expression is restricted to hair matrix and outer root sheath keratinocytes (Figure 1e and f). In early-catagen HFs, survivin expression decreased in the hair matrix and disappeared from the outer root sheath (Figure 1g). During mid-catagen, the number of survivin-positive cells further decreased in the regressing hair matrix (Figure 1h). Finally, in late catagen, only a few surviving-positive cells were detected in the regressing epithelial portion of the HF (Figure 1i). Because of the involvement of survivin in inhibiting apoptosis, co-visualization of survivin and apoptotic cells was also performed using commercially available Apo-Direct TUNEL Assay kit (Chemicon International Inc.). Lack of colocalization of survivin and TUNEL was detected in catagen HFs (Figure 1j). Collectively, these data suggested that survivin is involved in the maintenance of HF growth by supporting proliferation and protecting cells against apoptosis. It was recently shown that transcription of survivin is regulated by T-cell factor (TCF)/β-catenin signaling: TCF-binding sites were identified in the promoter region of survivin, and the dominant-negative TCF isoform was able to block survivin expression (Kim et al., 2003Kim P.J. Plescia J. Clevers H. Fearon E.R. Altieri D.C. Survivin and molecular pathogenesis of colorectal cancer.Lancet. 2003; 362: 205-209Abstract Full Text Full Text PDF PubMed Scopus (296) Google Scholar). The Wnt/β-catenin pathway plays key roles in HF growth and differentiation (DasGupta and Fuchs, 1999DasGupta R. Fuchs E. Multiple roles for activated LEF/TCF transcription complexes during hair follicle development and differentiation.Development. 1999; 126: 4557-4568Crossref PubMed Google Scholar; Van Mater et al., 2003Van Mater D. Kolligs F.T. Dlugosz A.A. Fearon E.R. Transient activation of beta-catenin signaling in cutaneous keratinocytes is sufficient to trigger the active growth phase of the hair cycle in mice.Genes Dev. 2003; 17: 1219-1224Crossref PubMed Scopus (208) Google Scholar), and we wished to clarify whether interactions between survivin and β-catenin are functional in the HF. By double immunostaining with antibodies against survivin and β-catenin (1:50; R&D Systems Inc., Minneapolis, MN), we observed that some cells expressing survivin in the hair matrix are also β-catenin-positive (Figure 2a–c). These data suggested that the expression of survivin in hair matrix keratinocytes may be under the control of and/or coordinated with Wnt/β-catenin signaling. To provide an experimental evidence for crosstalk between survivin and Wnt/β-catenin signaling in the HF, ICG-001 (Institute for Chemical Genomics, Seattle, WA), a small molecule that inhibits survivin transcription via blocking TCF/β-catenin binding to its co-activator CREB-binding protein (Emami et al., 2004Emami K.H. Nguyen C. Ma H. Kim D.H. Jeong K.W. Eguchi M. et al.A small molecule inhibitor of beta-catenin/CREB-binding protein transcription.Proc Natl Acad Sci USA. 2004; 101: 12682-12687Crossref PubMed Scopus (650) Google Scholar; Ma et al., 2005Ma H. Nguyen C. Lee K.S. Kahn M. Differential roles for the coactivators CBP and p300 on TCF/beta-catenin-mediated survivin gene expression.Oncogene. 2005; 24: 3619-3631Crossref PubMed Scopus (279) Google Scholar), was tested in HF organ culture model, as described previously (Philpott et al., 1994Philpott M.P. Sanders D. Westgate G.E. Kealey T. Human hair follicle growth in vitro: a model for the study of hair follicle biology.J Dermatol Sci. 1994; 7: S55-S72Abstract Full Text PDF PubMed Scopus (110) Google Scholar). ICG-001 was added to the microdissected anagen HFs from occipital human scalp skin derived from six different female donors (aged 45–55 years). To determine survivin protein content in the HFs treated with ICG-001, a commercially available ELISA kit was used (Assay Design Inc., Ann Arbor, MI). By ELISA, a significant decrease in the survivin protein levels were observed in the HFs after 1 μM ICG-001 treatment for 4 days, compared to vehicle control (P<0.001; Figure 2d). Concurrently, ICG-001 significantly reduced hair fiber elongation rate in a dose-dependent manner (P<0.0001; Figure 2e). However, ICG-001 did not cause premature catagen development in cultured HFs. Hair growth inhibition caused by ICG-001 treatment was accompanied by decrease in the number of proliferating (Ki-67+) cells and increase in the number of apoptotic (TUNEL+) cells in the hair bulb and the outer root sheath, compared to the controls (Figure 2f–i). These data are consistent with previous report on similar effects of ICG-001 (inhibition of proliferation and stimulation of apoptosis) associated with downregulation of survivin and increase of caspase-3 activity in several cell lines (Ma et al., 2005Ma H. Nguyen C. Lee K.S. Kahn M. Differential roles for the coactivators CBP and p300 on TCF/beta-catenin-mediated survivin gene expression.Oncogene. 2005; 24: 3619-3631Crossref PubMed Scopus (279) Google Scholar). However, very limited number of reports is available on the interactions between survivin and known regulators of apoptosis in the HF. Therefore, it would be very interesting to further explore and/or identify survivin upstream and downstream components in the control of proliferation and apoptosis in the HF. In summary, we provide the first evidence that (1) survivin is expressed in the proliferating keratinocytes of the hair matrix and outer root sheath of human anagen HF and its expression is decreased with the progression of catagen phase; (2) expression of survivin in anagen HF may be controlled by Wnt/β-catenin signaling. The dual functions of survivin may be involved in the control of the delicate proliferation–apoptosis balance controlling HF cyclic behavior. The authors state no conflict of interest." @default.
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• W2034642769 title "Survivin in the Human Hair Follicle" @default.
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