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TAGOHL, ..... (Topicals)

posted by TAGOHL, 09.04.2008, 23:37

Benji, thanks for the info -- very interesting. I need to ponder all this stuff. Here's a couple more abstracts. The first one is another recent genetic study which shows that a polymorphism in the ectodysplasin-A receptor gene is what gives Asians thick hair. The second study shows that ectodysplasin helps control the switch from anagen to catagen (early termination of anagen -- short growth cycles -- are a feature of MPB). Gene therapy for baldness would be really, really nice if it happens someday.

Hum Mol Genet. 2008 Mar 15;17(6):835-43.

A scan for genetic determinants of human hair morphology: EDAR is associated with Asian hair thickness.

Department of Human Genetics, Graduate School of Medicine, The University of Tokyo, Hongo, Tokyo, Japan.

Hair morphology is one of the most differentiated traits among human populations. However, genetic backgrounds of hair morphological differences among populations have not been clarified yet. In addition, little is known about the evolutionary forces that have acted on hair morphology. To identify hair morphology-determining genes, the levels of local genetic differentiation in 170 genes that are related to hair morphogenesis were evaluated by using data from the International HapMap project. Among highly differentiated genes, ectodysplasin A receptor (EDAR) harboring an Asian-specific non-synonymous single nucleotide polymorphism (1540T/C, 370Val/Ala) was identified as a strong candidate. Association studies between genotypes and hair morphology revealed that the Asian-specific 1540C allele is associated with increase in hair thickness. Reporter gene assays suggested that 1540T/C affects the activity of the downstream transcription factor NF-kappaB. It was inferred from geographic distribution of 1540T/C and the long-range haplotype test that 1540C arose after the divergence of Asians from Europeans and its frequency has rapidly increased in East Asian populations. These findings lead us to conclude that EDAR is a major genetic determinant of Asian hair thickness and the 1540C allele spread through Asian populations due to recent positive selection.

PMID: 18065779 [PubMed - in process]

Involvement of the Edar signaling in the control of hair follicle involution (catagen).

Department of Dermatology, Boston University School of Medicine, 609 Albany St., Boston, MA 02118, USA.

Ectodysplasin (Eda) and its receptor (Edar) are required for normal development of several ectodermal derivatives including hair follicles (HFs). Here, we show that during the murine hair cycle the expression of Eda A1, Edar, Edaradd, and TRAF6 transcripts are minimal in the resting phase and maximal during HF transition from active growth to regression (catagen). Eda A1 mRNA and Edar proteins were expressed in the hair matrix and outer and inner root sheaths of anagen HFs. During catagen, Eda A1 mRNA and Edar protein were expressed in the outer and inner root sheaths and later in the secondary hair germ. Catagen development accompanied by increased apoptosis in the outer root sheath was significantly accelerated in downless mice or after treatment of wild-type mice by a fusion protein that inhibits Edar signaling, compared with the corresponding controls. Microarray, real-time polymerase chain reaction, and immunohistochemical analyses of skin of downless mice revealed a strong decrease of expression of X-linked inhibitor of apoptosis protein (XIAP), compared with the controls, suggesting XIAP as a target for Edar signaling. Thus, our data demonstrate that in addition to its well-established role in HF morphogenesis, Edar signaling is also involved in hair cycle control and regulates apoptosis in HF keratinocytes during catagen.

PMID: 17148670 [PubMed - indexed for MEDLINE]


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