References: Hair growth and hair loss
Microsc Res Tech. 1997 Aug 15;38(4):443-51.
Morphological analysis of hair follicles in alopecia areata.
Tobin DJ.
Department of Biomedical Sciences, University of Bradford, England.
This study characterizes hair follicles from early alopecia areata lesions at both the light and electron microscopic levels and describes how affected hair follicles differ from normal hair growth. The study focuses on acute and active lesions where hair follicles show greatest divergence from the normal growth pattern and are most likely to display features of primary pathology. Morphologic analysis revealed regressive changes in the hair bulbs of anagen hair follicles in alopecia areata. While tissue injury did not appear to be cell type specific, pre-cortical keratinocytes and hair bulb melanocytes were primarily affected. Three distinct patterns of cell degeneration, of variable frequency, are described including "dark cell" transformation, apoptosis, and necrosis. Abnormal melanogenesis was a common finding in this study, which may explain some of the associated pigmentary anomalies seen clinically in acute alopecia areata. Tissue damage, which was not always associated with a mononuclear cell infiltrate, may explain the premature involution of suboptimal anagen hair follicles into an early resting phase in alopecia areata. Finally, scanning electron microscopic, light microscopic, and transmission electron microscopic studies describe defective cortex differentiation in characteristic "exclamation-mark" hair shafts. These hairs may result from a transient phase of cell degeneration among pre-cortical keratinocytes.
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Acta Derm Venereol. 1997 Sep;77(5):350-5.
Expression of retinoid nuclear receptor superfamily members in human hair follicles and its implication in hair growth.
Billoni N, Gautier B, Mahe YF, Bernard BA.
L' OREAL Advanced Research Laboratories. L' OREAL Hair Biology Research Group, Clichy, France.
Since clinical evidence of hair loss and hair depigmentation following etretinate therapy has been reported, we decided to study the expression levels of several members of the retinoid nuclear receptor superfamily in dermal and epithelial compartments of the human hair follicle. Additionally, we evaluated the effects of several ligands for these receptors on human hair growth in culture in vitro. We observed that the cellular/ cytoplasmic retinoic acid (RA) binding protein-II and the retinoid-X-receptor-alpha were constantly and strongly expressed in both compartments at levels comparable to those of vitamin D receptor. In dermal papilla cells, by contrast with RAR beta which was always expressed, RAR alpha and RAR gamma were not constantly expressed. In dermal sheath fibroblasts, both RAR alpha, RAR beta and RAR gamma mRNAs were moderately expressed, while in the epithelial compartment, namely the plucked hair, we observed the expression of the same genes in the absence of RAR beta. We also observed that RAR agonists all-trans RA and CD367 inhibited the survival of human hair follicles in culture in vitro, while RXR agonist CD2425 stimulated hair growth and survival at levels comparable to those of 1 alpha,25-dihydroxyvitamin D3, suggesting that RXR agonists might stimulate hair growth in humans in vivo.
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The in vitro growth of human hair follicles is inhibited by interleukin (IL)-1 beta and phorbol esters, such as phorbol-myristate-acetate (PMA), but enhanced by insulin-like growth factor (IGF)-I. Although this process is only incompletely understood, the dermal papilla as a pivotal part of the hair follicle is almost certainly involved. Since protein kinase C (PKC) isoenzymes are activated by phorbol esters and are key enzymes in signalling pathways of several hormones, neurotransmitters, and growth factors, we addressed the question whether the action of the above-mentioned hair growth-modulating substances may affect PKC isoenzymes in cultured dermal papilla cells (DPC). By Western blot analysis, protein kinase C alpha, -epsilon, -gamma, -iota, -lambda, and the RACK1 receptor protein were detected in dermal papilla cell cultures, whereas the isoenzymes delta and mu were expressed only at low levels and protein kinase C-beta, -theta, and -zeta, were not present. After PMA stimulation, the PKC alpha, -epsilon, and -gamma were translocated from the cytosol to the membrane fraction and subsequently down-regulated. PKC iota was down-regulated but not translocated, and PKC lambda and RACK1 were not affected by PMA. Neither, IL-1 beta nor IGF had an effect on PKC or RACK1 expression. We conclude that cultured DPC express a distinct PKC isoenzyme pattern and that the PMA-induced growth arrest in cultivated hair follicles may be transmitted via protein kinases, whereas the effects of IL-1 beta or IGF may be transduced via other signal transduction pathways or other cell types.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9298128&dopt=Abstract
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