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Pathogen research abs 1 || Pathogen research abs 2 || Pathogen research abs 3 || Pathogen research abs 4 || Pathogen research abs 5 || Hormone and endocrine research abs 1 || Hormone and endocrine research abs 2 || Hormone and endocrine research abs 3 || Hormone and endocrine research abs 4 || Hormone and endocrine research abs 5 || Follicle and follicular cells research abs 1

J Investig Dermatol Symp Proc. 2003 Jun;8(1):80-6.
Plasticity and cytokinetic dynamics of the hair follicle mesenchyme during the hair growth cycle: implications for growth control and hair follicle transformations.

Tobin DJ, Gunin A, Magerl M, Paus R.

Department of Biomedical Sciences, School of Life Sciences, University of Bradford, Bradford, West Yorkshire, UK. dtobiradford.ac.uk

Hair fiber production is the macroscopic end-point of a highly complex set of interactions between the hair follicle's epithelial and mesenchymal components. The nature of this relationship is largely set during hair follicle morphogenesis, but is dramatically revisited in the adult during the unique tissue remodeling events required for hair follicle cycling. Whereas significant attention has focused on the fate of the hair follicle epithelium during these events, associated changes in hair follicle fibroblast subpopulations remain unclear. Here, we present a speculative review that represents a critical and innovative synthesis of the current literature and summarizes a recently submitted original study by the authors, on the nature of hair cycle-dependent fibroblast dynamics and on how perturbations thereof may lead to several clinical manifestations of altered human hair growth.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12895000&dopt=Abstract [PubMed - in process]

J Investig Dermatol Symp Proc. 2003 Jun;8(1):91-5.
Label-retaining cells (presumptive stem cells) of mice vibrissae do not express gap junction protein connexin 43.

Matic M, Simon M.

Department of Oral Biology and Pathology, Health Science Center, SUNY at Stony Brook, NY 11794, USA. mmatinotes.cc.sunysb.edu

We investigated whether connexin 43, a gap junction protein present in human epidermis and mouse hair follicle, can serve as a negative marker for keratinocyte stem cells. Experiments carried out in mouse pelage and vibrissae hair follicles demonstrated that most of the slowly cycling cells, detected as label-retaining cells, do not express connexin 43. In humans, cells with immunohistochemically undetectable levels of connexin 43 are found in the epidermal basal layer of neonatal foreskin, and in the follicular bulge region. About 10% of the basal keratinocytes are connexin 43 negative, as determined by flow cytometry. These cells are uniformly small and low in granularity suggesting that presumptive keratinocyte stem cells can be identified and separated based on connexin 43 expression.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12895002&dopt=Abstract [PubMed - in process]

J Investig Dermatol Symp Proc. 2003 Jun;8(1):96-9.
Characterization of human keratin-associated protein 1 family members.

Shimomura Y, Aoki N, Rogers MA, Langbein L, Schweizer J, Ito M.

Department of Dermatology, Niigata University School of Medicine, Niigata, Japan. yshimed.niigata-u.ac.jp

Keratin-associated proteins are involved in the formation of the cross-linked network of the keratin-intermediate filament proteins that support hair fibers. In recent years, several keratin-associated protein genes have been identified and become an attractive topic in hair research. More recently, we isolated two cDNA encoding novel members of the human keratin-associated protein 1 family (human keratin-associated protein 1.6 and human keratin-associated protein 1.7), and described their expression in the hair follicle by RNA in situ hybridization. A comparison of human keratin-associated protein 1.6 and human keratin-associated protein 1.7 with other human keratin-associated protein 1 members revealed that keratin-associated protein 1 proteins are fundamentally composed of five distinct domains, and that they can be classified primarily by a striking variation in double cysteine-containing pentapeptide repeats in the repetitive I domain. The sum of the data analyzed suggests that human keratin-associated protein 1 family genes may have arisen mainly through gene duplication of the cysteine-repeat motifs during evolution.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12895003&dopt=Abstract [PubMed - in process]

J Investig Dermatol Symp Proc. 2003 Jun;8(1):100-3.
The distribution of estrogen receptor beta is distinct to that of estrogen receptor alpha and the androgen receptor in human skin and the pilosebaceous unit.

Thornton MJ, Taylor AH, Mulligan K, Al-Azzawi F, Lyon CC, O'Driscoll J, Messenger AG.

Department of Biomedical Sciences, University of Bradford, Bradford, West Yorkshire, UK. M.J.Thortoradford.ac.uk

Both estrogens and androgens play important parts in skin and hair physiology, although studies of estrogen action in human skin have been rather limited. Recently, a second estrogen receptor (beta) has been identified in many nonclassical target tissues, including androgen-dependent tissues. Therefore, we have revisited the role of estrogens in human skin and hair by comparing the pattern of expression by immunohistochemistry for both estrogen receptors (alpha and beta) and the androgen receptor. Immunolocalization of androgen receptors was only seen in hair follicle dermal papilla cells and the basal cells of the sebaceous gland. Little specific staining of estrogen receptor alpha was seen anywhere except the sebaceous gland. In contrast estrogen receptor beta was highly expressed in epidermis, blood vessels, and dermal fibroblasts, whereas in the hair follicle it was localized to nuclei of the outer root sheath, epithelial matrix, and dermal papilla cells. Serial sections also showed strong nuclear expression of estrogen receptor beta in the cells of the bulge, whereas neither estrogen receptor alpha or androgen receptor was expressed. In the sebaceous gland, estrogen receptor beta was expressed in both basal and partially differentiated sebocytes in a similar pattern to estrogen receptor alpha. There was no obvious difference in the expression of either estrogen receptor in male or female nonbalding scalp skin. The results of this immunohistochemical study propose that estrogen receptor beta and not estrogen receptor alpha is the main mediator of estrogen action in human skin and the hair follicle. Further studies with androgen-dependent skin are required to determine whether estrogen receptor beta has a regulatory role on androgen receptor expression in the hair follicle in parallel with its role in other androgen-dependent tissues.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12895004&dopt=Abstract [PubMed - in process]

J Investig Dermatol Symp Proc. 2003 Jun;8(1):104-8.
Fas-deficient C3.MRL-Tnfrsf6(lpr) mice and Fas ligand-deficient C3H/HeJ-Tnfsf6(gld) mice are relatively resistant to the induction of alopecia areata by grafting of alopecia areata-affected skin from C3H/HeJ mice.

Freyschmidt-Paul P, McElwee KJ, Botchkarev V, Kissling S, Wenzel E, Sundberg JP, Happle R, Hoffmann R.

Department of Dermatology, Philipp University, Marburg, Germany. freyschailer.uni-marburg.de

Alopecia areata is suspected to be a T cell-mediated autoimmune disease of the hair follicle, where Fas is expressed on hair follicles and Fas ligand on perifollicular infiltrates. To elucidate whether the Fas/Fas ligand pathway is of pathogenetic significance in alopecia areata, we investigated whether alopecia areata can be induced in Fas-deficient and Fas ligand-deficient mice and whether alopecia areata develops in Fas-deficient and Fas ligand-deficient skin. Therefore, we induced alopecia areata by grafting alopecia areata-affected C3H/HeJ mouse skin on to C3H/HeJ mice (control), on to Fas ligand-deficient C3H/HeJ-Tnfsf6(gld) mice or Fas-deficient C3.MRL-Tnfrsf6(lpr) mice. All control mice developed alopecia areata, whereas no Fas-deficient mice showed hair loss and two of seven Fas ligand-deficient mice developed only transitory, limited alopecia areata. Moreover, skin from C3H/HeJ mice (control), C3H/HeJ-Tnfsf6(gld) mice, and C3.MRL-Tnfrsf6(lpr) mice was grafted on to C3H/HeJ mice with extensive alopecia areata. Skin grafts from control mice developed hair loss, whereas Fas-deficient and Fas ligand-deficient skin grafts were spared from alopecia areata. Terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end-labeling and immunofluorescence studies revealed an increased number of apoptotic cells and expression of Fas on hair follicles as well as expression of Fas ligand on cells of the perifollicular infiltrate in C3H/HeJ mice with alopecia areata, whereas in Fas-deficient and Fas ligand-deficient mice apoptotic cells were virtually absent in hair follicles. The results suggest that the Fas/Fas ligand pathway plays an important pathogenetic role in alopecia areata.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12895005&dopt=Abstract [PubMed - in process]

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