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J Eur Acad Dermatol Venereol. 2008 Aug 13. [Epub ahead of print]Click here to read Links
Proliferation, DNA repair and apoptosis in androgenetic alopecia.
El-Domyati M, Attia S, Saleh F, Bassyouni M, El-Fakahany H, Abdel-Wahab H.
Department of Dermatology, Faculty of Medicine, Al-Minya University, Al-Minya, Egypt.
Background Androgenetic alopecia is a common hair disorder, resulting from interplay of genetic, endocrine and ageing factors. Meanwhile, it is unclear if an altered degree of proliferation or increased apoptosis could contribute to its pathogenesis. Objective To evaluate the role of proliferation, DNA damage and apoptosis in the pathogenesis of androgenetic alopecia. Methods Thirty biopsies were taken from the frontal (bald) area and occipital (hairy) area of 15 male patients with androgenetic alopecia, as well as five specimens from frontal area of five age-matched controls. These specimens were used for immunohistochemical staining of cell proliferation [proliferating cell nuclear antigen (PCNA)] and DNA repair markers (XRCC1, APE1, PARP-1) as well as apoptosis regulatory protein p53. Results The frontal bald area of patients showed significantly higher levels of X-ray Cross Complementing-1 (XRCC1; P < 0.001) and p53 (P < 0.001) expression when compared with occipital hairy area of patients and frontal area of controls (P = 0.003 and 0.04, respectively). On the other hand, there were significantly lower expression of PCNA (P < 0.001) and apurinic/apyridinic endonuclease 1 (APE1; P = 0.001 and 0.02) when compared with the frontal area of controls and occipital area of patients, respectively. Meanwhile, APE1 showed significant inverse correlation with p53 overexpression (P = 0.03). Conclusion 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. An alternative pathway would take place in order to eliminate the damaged cells through apoptosis.
Nothing too surprising here. More confirmation that hair follicles are damaged at the cellular level which probably strengthens the notion that there is some sort of oxidative process that is damaging cells and this in turn leads to a higher rate of cell death. There is potentially more interesting in specific stuff in the different expression levels of the DNA repair markers (XRCC1 is upregulated while APE1 is downregulated) and their implications but I dont have time to read the whole thing and look all that stuff up right now.
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Proliferation, DNA repair and apoptosis in androgenetic alopecia.
El-Domyati M, Attia S, Saleh F, Bassyouni M, El-Fakahany H, Abdel-Wahab H.
Department of Dermatology, Faculty of Medicine, Al-Minya University, Al-Minya, Egypt.
Background Androgenetic alopecia is a common hair disorder, resulting from interplay of genetic, endocrine and ageing factors. Meanwhile, it is unclear if an altered degree of proliferation or increased apoptosis could contribute to its pathogenesis. Objective To evaluate the role of proliferation, DNA damage and apoptosis in the pathogenesis of androgenetic alopecia. Methods Thirty biopsies were taken from the frontal (bald) area and occipital (hairy) area of 15 male patients with androgenetic alopecia, as well as five specimens from frontal area of five age-matched controls. These specimens were used for immunohistochemical staining of cell proliferation [proliferating cell nuclear antigen (PCNA)] and DNA repair markers (XRCC1, APE1, PARP-1) as well as apoptosis regulatory protein p53. Results The frontal bald area of patients showed significantly higher levels of X-ray Cross Complementing-1 (XRCC1; P < 0.001) and p53 (P < 0.001) expression when compared with occipital hairy area of patients and frontal area of controls (P = 0.003 and 0.04, respectively). On the other hand, there were significantly lower expression of PCNA (P < 0.001) and apurinic/apyridinic endonuclease 1 (APE1; P = 0.001 and 0.02) when compared with the frontal area of controls and occipital area of patients, respectively. Meanwhile, APE1 showed significant inverse correlation with p53 overexpression (P = 0.03). Conclusion 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. An alternative pathway would take place in order to eliminate the damaged cells through apoptosis.
Nothing too surprising here. More confirmation that hair follicles are damaged at the cellular level which probably strengthens the notion that there is some sort of oxidative process that is damaging cells and this in turn leads to a higher rate of cell death. There is potentially more interesting in specific stuff in the different expression levels of the DNA repair markers (XRCC1 is upregulated while APE1 is downregulated) and their implications but I dont have time to read the whole thing and look all that stuff up right now.
hh