Proliferation, DNA repair and apoptosis in androgenetic alopecia

El‐Domyati, Moetaz; Attia, Sameh K.; Saleh, Fatma; Bassyouni, MI; El-Fakahany, Hasan; Abdel-Wahab, Hossam

doi:10.1111/j.1468-3083.2008.02937.x

Cited by 21 publications

(19 citation statements)

References 33 publications

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“…altered degree of proliferation or increased apoptosis could contribute to its pathogenesis. Domyati et al (2009) reported that the frontal (bald) area of patients with androgenetic alopecia has lower proliferation rate that result in follicular miniaturization. There is increased DNA damage that would be beyond the capacity of cells to repair in advanced cases.…”

Section: Discussionmentioning

confidence: 98%

Fructus panax ginseng extract promotes hair regeneration in C57BL/6 mice

Park

Shin

2011

Journal of Ethnopharmacology

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Section: Discussionmentioning

confidence: 98%

Fructus panax ginseng extract promotes hair regeneration in C57BL/6 mice

Park

Shin

2011

Journal of Ethnopharmacology

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“…Thus, the abnormalities in the hair follicles of androgenetic alopecia are consistent with the purported pathophysiologic mechanisms of the condition, implying miniaturization (atrophy or lower depth) of the hair follicle with the predominant involvement of the frontal region. Hair follicle shrinkage with a progressive decrease in the proportion during the mature (anagen) stage was previously linked to a decreased proliferation rate of follicular keratinocytes 14 . Whether the primary cause is vascular dysfunction or local deficits in follicular trophic factors is currently unknown.…”

Section: Discussionmentioning

confidence: 99%

Hair Morphology in Androgenetic Alopecia

Wortsman

Guerrero

Wortsman

2014

J of Ultrasound Medicine

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Sonographic and Electron Microscopic Studiesesides the esthetic connotations, hair serves important roles in cutaneous functions such as dispersion of sweat gland products and regulation of body temperature. 1 Hair loss, or alopecia, is therefore clinically important as it may be also associated with psychologic disturbances from disruptions of the selfimage of affected patients. 2 Since hair loss may imply hair fragility or structural abnormalities, a detailed morphologic evaluation should be an important step for studying its pathologic characteristics and supporting management. In this regard, recent developments in the field of sonography have allowed details of the hair anatomy to be uncovered. 3 On sonography, normal scalp hair follicles appear as oblique hypoechoic bands in the dermis, extending to variable depths according to the hair cycle phase; thus, active hair follicles (anagen phase) are located both in the superficial and deep dermis and can even reach the upper hypodermis, whereas inactive hair Objectives-To assess hair morphology in androgenetic alopecia on sonography and electron microscopy.Methods-A prospective study was performed in 33 patients with androgenetic alopecia and 10 unaffected control participants. In vivo sonography of the hair follicles of the scalp and in vitro sonography and electron microscopy of the hair shafts were performed according to a standardized protocol that included analysis of the right frontal and occipital regions. The upper frequency limit of the ultrasound probes ranged between 15 and 18 MHz.Results-Scalp hair follicles and hair shafts were recognizable on sonography in all cases. Hair follicles in alopecia cases had significantly lower depths (P < .05). The hair shafts in alopecia also had a different distribution of their laminar pattern on in vitro sonography, with a greater presence of mixed (trilaminar and bilaminar) and solely bilaminar tracts in comparison with the controls (mostly trilaminar). On electron microscopy, the alopecia hair tracts showed irregularities and commonly a "melted candle" appearance of the cuticle.Conclusions-Sonography and electron microscopy uncover distinct abnormalities in the morphology of hair in androgenetic alopecia, which may potentially support the diagnosis and management of this common condition.

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“…Molecular epidemiologic studies have identified associations between polymorphisms in genes involved in DNA-repair pathways and increased risk of various types of cancers, including lung cancer (16 -21). However, when DNA damage is extensive and beyond the capacity of cells to repair, cell replacement through apoptosis may be a preferred alternative to DNA repair (22). So, there exists the possibility that high expression of DNA-repair genes may coincide with resistance to apoptosis on cellular stress like unrepairable DNA damage, therefore contributing to cancer risk.…”

Section: Discussionmentioning

confidence: 99%

Functional characterization of a promoter polymorphism inAPE1/Ref‐1that contributes to reduced lung cancer susceptibility

et al. 2009

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Apurinic/apyrimidinic endonuclease 1/redox effector factor-1 (APE1/Ref-1) is a ubiquitous multifunctional protein that possesses both DNA-repair and redox regulatory activities. Although it was originally identified as a DNA-repair enzyme, accumulating evidence supports a role of APE1/Ref-1 in tumor development. To investigate association between APE1/Ref-1 polymorphisms and lung cancer risk in Chinese populations, we first genotyped three variants of APE1/Ref-1 and found a -141 T-to-G variant (rs1760944) in the promoter associated with decreased risk of lung cancer [odds ratio (OR) = 0.62 for GG; P=0.043]. Similar results were obtained in a follow-up replication study. Combined data from the two studies comprising a total of 1072 lung cancer patients and 1064 cancer-free control participants generated a more significant association (P=0.002). We observed lower APE1/Ref-1 mRNA levels in the presence of the protective G allele in human peripheral blood mononuclear cells and normal lung tissues. The -141G-allele-promoter construct exhibited decreased luciferase reporter gene expression. Electrophoretic mobility shift assays and surface plasmon resonance analysis showed that the -141G allele impaired the binding affinity of some transcription factor, accounting for lower APE1/Ref-1-promoter activity. Supershift assays further revealed that the protein of interest was octamer-binding transcription factor-1 (Oct-1). Chromatin immunoprecipitation reconfirmed binding of Oct-1 to the APE1/Ref-1 -141-promoter region. We also found that Oct-1 conferred attenuated transactivation capacity toward the -141G variant by exogenously introducing Oct-1. These data indicate that genetic variations in APE1/Ref-1 may modify susceptibility to lung cancer and provide new insights into an unexpected effect of APE1/Ref-1 on lung carcinogenesis.

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Proliferation, DNA repair and apoptosis in androgenetic alopecia

Cited by 21 publications

References 33 publications

Fructus panax ginseng extract promotes hair regeneration in C57BL/6 mice

Fructus panax ginseng extract promotes hair regeneration in C57BL/6 mice

Hair Morphology in Androgenetic Alopecia

Functional characterization of a promoter polymorphism inAPE1/Ref‐1that contributes to reduced lung cancer susceptibility

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