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J Dermatol Sci. 2008 Jul 17. [Epub ahead of print]Click here to read Links
Ephrin-A3 not only increases the density of hair follicles but also accelerates anagen development in neonatal mice.
Yamada Y, Midorikawa T, Oura H, Yoshino T, Ohdera M, Kubo Y, Arase S.
Biological Science Research Center, Lion Corporation, Kanagawa 256-0811, Japan; Department of Dermatology, Institute of Health Biosciences, The University of Tokushima Graduate School, Tokushima 770-8503, Japan.
BACKGROUND: Ephrins are cell-membrane-bound ligands for Eph receptor tyrosine kinases (Eph). Although ephrins are known to regulate a variety of developmental processes, little is known of their role in hair development. Previously, we studied the gene expression of dermal papilla cells from androgenetic alopecia and found that ephrin-A3 was significantly down-regulated. OBJECTIVE: To characterize the expression of ephrin-A3 in the hair cycle and evaluate the effect of ephrin-A3 on hair growth. METHODS: We investigated gene expression and protein expression of each ephrin-As and EphAs in the skin of neonatal mice through the first and second hair cycle using quantitative PCR and immunohistochemical analysis, respectively. We also injected ephrin-A3 protein into the skin of neonatal mice and demonstrated the effect of ephrin-A3 on hair follicle development. RESULTS: Expression of ephrin-A3 revealed a rapid increase at the beginning of the anagen phase, a peak during the mid-anagen, and a rapid fading during the telogen phase. In addition, we found ephrin-A3 protein was expressed in the developing hair follicles with a characteristic spatiotemporal localization. Furthermore, injection of ephrin-A3 into the skin of neonatal
mice markedly accelerated the differentiation process of hair follicles. In addition, injection of ephrin-A3 unexpectedly increased the number of hair follicles. CONCLUSION: These findings demonstrated that ephrin-A3 not only accelerates anagen development but also increases the density of hair follicles, and also suggested that an ephrin-A-EphA signal pathway is closely involved in hair follicle development.
Given that there is less hair in anagen in Androgenetic Alopecia and more hair in telogen that could well explain why ephrin-A3 is downregulated given that it is found to be exprssed much higher in anagen. Still the fact that in newborn mice the injection of ephrin increased the number of hair follciles indicate that there may be more to its downregulation in male pattern baldness and that it would probably join the list of things that help the Follica process create new hair follicles along with increased EDAR signalling, increased wnt signalling, minoxidil etc.
hh
Ephrin-A3 not only increases the density of hair follicles but also accelerates anagen development in neonatal mice.
Yamada Y, Midorikawa T, Oura H, Yoshino T, Ohdera M, Kubo Y, Arase S.
Biological Science Research Center, Lion Corporation, Kanagawa 256-0811, Japan; Department of Dermatology, Institute of Health Biosciences, The University of Tokushima Graduate School, Tokushima 770-8503, Japan.
BACKGROUND: Ephrins are cell-membrane-bound ligands for Eph receptor tyrosine kinases (Eph). Although ephrins are known to regulate a variety of developmental processes, little is known of their role in hair development. Previously, we studied the gene expression of dermal papilla cells from androgenetic alopecia and found that ephrin-A3 was significantly down-regulated. OBJECTIVE: To characterize the expression of ephrin-A3 in the hair cycle and evaluate the effect of ephrin-A3 on hair growth. METHODS: We investigated gene expression and protein expression of each ephrin-As and EphAs in the skin of neonatal mice through the first and second hair cycle using quantitative PCR and immunohistochemical analysis, respectively. We also injected ephrin-A3 protein into the skin of neonatal mice and demonstrated the effect of ephrin-A3 on hair follicle development. RESULTS: Expression of ephrin-A3 revealed a rapid increase at the beginning of the anagen phase, a peak during the mid-anagen, and a rapid fading during the telogen phase. In addition, we found ephrin-A3 protein was expressed in the developing hair follicles with a characteristic spatiotemporal localization. Furthermore, injection of ephrin-A3 into the skin of neonatal
mice markedly accelerated the differentiation process of hair follicles. In addition, injection of ephrin-A3 unexpectedly increased the number of hair follicles. CONCLUSION: These findings demonstrated that ephrin-A3 not only accelerates anagen development but also increases the density of hair follicles, and also suggested that an ephrin-A-EphA signal pathway is closely involved in hair follicle development.
Given that there is less hair in anagen in Androgenetic Alopecia and more hair in telogen that could well explain why ephrin-A3 is downregulated given that it is found to be exprssed much higher in anagen. Still the fact that in newborn mice the injection of ephrin increased the number of hair follciles indicate that there may be more to its downregulation in male pattern baldness and that it would probably join the list of things that help the Follica process create new hair follicles along with increased EDAR signalling, increased wnt signalling, minoxidil etc.
hh