Expression of beta-catenin, p63 and CD34 in hair follicles during the course of androgenetic alopecia

Abstract

During the hair growth cycle, the hair follicle appears to recapitulate part of its embryogenesis where both beta-catenin and p63 participate. The aim of the present study was to investigate the hypothesis that beta-catenin and p63 protein may be involved in the pathogenesis of androgenetic alopecia. Second, expression of CD34 protein was used to assess the capillary density of the affected skin. Cadavers were used as samples and the results showed that analysis of beta-catenin, p63 and CD34 expressions in human cadaverous scalp skin by immunohistochemical techniques were possible. We detected a higher expression of p63 in occipital skin in comparison to the affected frontal areas. However, we found only minimal changes in beta-catenin expression comparing frontal and occipital areas. A completely new finding was the expression of CD34 positive cells in the outer root sheath of hair follicles.

p63 immunoexpression in hair follicles of normal and alopecia X‐affected skin of Pomeranian dogs

“…The immunohistochemical evaluation of p63 expression in our cases revealed a pattern similar to the results obtained in human skin and HFs by Fiuraskova et al, 14 in which the outer root sheaths from normal occipital skin had significantly higher expression of p63 in comparison with frontal alopecic areas of AGA‐affected human patients. A greater number of cases with biopsy samples in clinically unaffected/hypotrichotic areas would clarify whether p63 immunoexpression in these areas significantly differs from normal control cases and clinically alopecic areas.…”

Hedgehog signaling maintains hair follicle stem cell phenotype in young and aged human skin

“…For instance, as opposed to the mouse HFSC niche, the so‐called bulge for its protuberance, the human ‘bulge’ is less morphologically distinct. In addition, certain genes that are used as specific mouse HFSC markers, such as CD34 or p63, are not limited to HFSCs in human skin (Fiuraskova et al. , 2005).…”

A TP63 Mutation Causes Prominent Alopecia with Mild Ectodermal Dysplasia

“…Thus, differences in clinical manifestations associated with EEC, ADULT, or p.Trp192Arg DBD mutations might result from the distinct effects of these mutant proteins on the transactivation of p63 target genes. The p.Trp192Arg mutation could predominantly affect the transactivation of p63 target genes previously involved in hair follicle growth, thus explaining the observed phenotype with prominent alopecia and minor ectodermal anomalies (Clements et al, 2012;Fiuraskova et al, 2005;Romano et al, 2010).…”