EGF acts as an ON/OFF swtich!

http://www.jbc.org/cgi/reprint/278/28/26120.pdf

The hair growth cycle consists of three stages known as the anagen (growing), catagen (involution), and telogen (resting) phases. This cyclical growth of hair is regulated by a diversity of growth factors. Although normal expression of both epidermal growth factor and its receptor (EGFR) in the outer root sheath is down-regulated with the completion of follicular growth, here we show that continuous expression of epidermal growth factor in hair follicles of transgenic mice arrested follicular development at the final stage of morphogenesis. Data from immunoprecipitation and immunoblotting showed that epidermal growth factor signals through EGFR/ErbB2 heterodimers in skin. Furthermore, topical application of tyrphostin AG1478 or AG825, specific inhibitors of EGFR and ErbB2, respectively, completely inhibited new hair growth in wild type mice but not in transgenic mice. When the transgenic mice were crossed with waved-2 mice, which possess a lower kinase activity
of EGFR, the hair phenotype was rescued in the offspring. Taken together, these data suggest that EGFR signaling is indispensable for the initiation of hair growth. On the other hand, continuous expression of epidermal growth factor prevents entry into the catagen phase. We propose that epidermal growth factor functions as a biologic switch that is turned on and off in hair follicles at the beginning and end of the anagen phase of the hair cycle, guarding the entry to and exit from the anagen phase.

» http://www.jbc.org/cgi/reprint/278/28/26120.pdf
»
» The hair growth cycle consists of three stages known as the anagen
» (growing), catagen (involution), and telogen (resting) phases. This
» cyclical growth of hair is regulated by a diversity of growth factors.
» Although normal expression of both epidermal growth factor and its
» receptor (EGFR) in the outer root sheath is down-regulated with the
» completion of follicular growth, here we show that continuous expression of
» epidermal growth factor in hair follicles of transgenic mice arrested
» follicular development at the final stage of morphogenesis.
Data from
» immunoprecipitation and immunoblotting showed that epidermal growth factor
» signals through EGFR/ErbB2 heterodimers in skin. Furthermore, topical
» application of tyrphostin AG1478 or AG825, specific inhibitors of EGFR and
» ErbB2, respectively, completely inhibited new hair growth in wild type mice
» but not in transgenic mice. When the transgenic mice were crossed with
» waved-2 mice, which possess a lower kinase activity
» of EGFR, the hair phenotype was rescued in the offspring. Taken
» together, these data suggest that EGFR signaling is indispensable for the
» initiation of hair growth.
On the other hand, continuous expression of
» epidermal growth factor prevents entry into the catagen phase. We
» propose that epidermal growth factor functions as a biologic switch that is
» turned on and off in hair follicles at the beginning and end of the anagen
» phase of the hair cycle, guarding the entry to and exit from the anagen
» phase.

What does this mean for us? Is this along with the science that is involved Follica?

It’s not rock-solid proof of anything. But it’s another suggestion that Folica is onto something in general.

Inhibiting the EGF-R signal is the primary thing happening (other than just natural wounding) in the Folica method.

» It’s not rock-solid proof of anything. But it’s another suggestion that
» Folica is onto something in general.
»
»
» Inhibiting the EGF-R signal is the primary thing happening (other than
» just natural wounding) in the Folica method.

In meanwhile. Its 2008 and we are still bald.