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Hair Follicle Stem Cells (hair + follicle_stem_cell)
Selected AbstractsDefining the hair follicle stem cell (Part II)JOURNAL OF CUTANEOUS PATHOLOGY, Issue 10 2009Peggy Myung MD [source] Etiology of cicatricial alopecias: a basic science point of viewDERMATOLOGIC THERAPY, Issue 4 2008Kevin J. McElwee ABSTRACT: This article presents a short summary of our current knowledge of cicatricial alopecia disease pathogenesis and the hypothetical disease mechanisms that may be involved in scarring alopecia development. Several forms of scarring alopecia likely involve targeted cytotoxic action against hair follicle cells mediated by a folliculocentric inflammation. However, the specific nature of the inflammatory interference in hair follicle growth is open to question. A popular hypothesis of lymphocyte-mediated scarring alopecia development involves autoimmune targeting of hair follicle,specific self-antigens, although there is no direct evidence in support of such a view. Alternative hypotheses focus on defects in sebaceous gland function, destruction of hair follicle stem cells, and interference in the communication between hair follicle mesenchyme and epithelium. Many questions arise from these hypotheses, and addressing them with a systematic research approach may enable significant advances in understanding cicatricial alopecia etiology. [source] Multipotent nestin-expressing hair follicle stem cellsTHE JOURNAL OF DERMATOLOGY, Issue 1 2009Yasuyuki AMOH First page of article [source] Cytokeratin 15 expression in apocrine mixed tumors of the skin and other benign neoplasms with apocrine differentiationTHE JOURNAL OF DERMATOLOGY, Issue 1 2006Noriyuki MISAGO ABSTRACT To clarify the features of apocrine mixed tumors (AMT) of the skin among benign neoplasms with apocrine differentiation in their relationship to follicular stem cells, we investigated the immunohistochemical expression of CK15 (LHK15 and C8/144B), which is a relatively specific marker of hair follicle stem cells in the bulge, in 35 cases of eight different benign neoplasms with presumed apocrine differentiation. All eight cases of AMT of the skin showed CK15 immunostaining of the neoplastic cells, and all four cases of syringocystadenoma papilliferum, all five cases of spiradenoma, and both cases of cylindroma also showed a focally positive reaction to CK15. None of the other benign neoplasms with presumed apocrine differentiation showed CK15 expression. In AMT of the skin, the proportion of CK15-positive cells in the follicular or sebaceous differentiation group (78.8%, average of four cases) was significantly higher than the group without this differentiation (8.8%, average of four cases). AMT of the skin are unique among benign neoplasms with apocrine differentiation in their substantial and constant CK15 expression, suggesting that they derive from multipotent epithelial stem cells in the bulge. AMT of the skin with follicular or sebaceous differentiation are considered to show an immature stage of apocrine differentiation still rich in stem cells or to originate from stem cells with an incompletely established apocrine fate. The partially positive reaction for CK15 in syringocystadenomas papilliferum and spiradenoma/cylindroma may depend on the ability to express CK15 in stem cells with an apocrine fate or result from the follicular and apocrine nature of this neoplasm. [source] Lhx2,decisive role in epithelial stem cell maintenance, or just the "tip of the iceberg"?BIOESSAYS, Issue 12 2006Stephan Tiede Stem cell self renewal, maintenance and differentiation are influenced by the convergence of intrinsic cellular signals and extrinsic microenvironmental cues from the surrounding stem cell niche. However, the specific signals involved are often still poorly understood. This is also true for skin epithelial stem cells. Recently, by transcriptionally profiling of embryonic hair progenitors in mice, Rhee et al.1 have managed to define how murine hair follicle epithelial stem cells are specified and maintained in an undifferentiated state. These authors have identified Lhx2 as a transcription factor functionally positioned downstream of signals necessary to specify hair follicle stem cells such as p63 or NF,B, but upstream of signals like Wnt/,-catenin, Bmp or Shh that are required to drive activated stem cells via the production of transient amplifying cells into terminal differentiation. BioEssays 28: 1157,1160, 2006. © 2006 Wiley Periodicals, Inc. [source] Caveolin-1 is expressed on multipotent cells of hair follicles and might be involved in their resistance to chemotherapyBRITISH JOURNAL OF DERMATOLOGY, Issue 3 2005S. Selleri Summary Background, Caveolin-1 is the principal protein that composes caveolae, which are vesicular invaginations present on the plasma membrane of different cell types. Caveolae are involved in a variety of cellular functions including regulation of proliferation rate and resistance to chemotherapeutic drugs. Chemotherapy frequently induces alopecia which is reversible most probably due to the low proliferative rate of hair follicle stem cells and due to the expression of proteins which confer resistance. Objectives, Using a specific animal model and immunohistochemistry, we analysed the expression of both caveolin-1 and the cell proliferation marker ,-catenin, at different stages of the hair follicle cycle, both before and after doxorubicin (DXR) -induced alopecia. Methods, Seven-week-old C57BL/6 mice were depilated in order to synchronize hair follicle cycle in the anagen phase. Chemotherapy with DXR 15 mg kg,1 was used to induce alopecia. Control and treated mice were then sacrificed at precise time points and caveolin-1 expression in hairs at different stages of the cycle were analysed by immunohistochemistry. By double immunofluorescence, colocalization of caveolin-1 and cytokeratin-15 was confirmed in the bulge region. The state of proliferation of cells composing hair follicle was assessed by ,-catenin immunohistochemistry. Results, Caveolin-1 was expressed by the cells of the bulge area, the multipotent compartment of the hair follicle, during all phases of growth (anagen), regression (catagen) and resting (telogen). During the anagen phases, nuclear ,-catenin labelling was not observed in bulge cells, but rather in the deeper portion of the follicle. Damaged hair follicles from DXR-treated mice presented bulge cells which still expressed caveolin-1, suggesting that this protein might play a role in their drug resistance. As expected, no ,-catenin nuclear staining was detectable in DXR-treated hair follicles, indicating the complete lack of proliferative processes. The differential localization of caveolin-1 and ,-catenin suggests that the mutually exclusive expression of these proteins is useful for correct hair regrowth, whether during the physiological cycle or after chemotherapy-induced alopecia. Conclusions, Expression of caveolin-1 within the multipotent cell compartment of the hair follicle can explain the resistance of bulge cells to many chemotherapeutics, suggested by the reversibility of chemotherapy-induced alopecia. [source] | ||||||||||