by Kevin Rands | May 13, 2016 4:17 am
The following is a review by Kevin J. McElwee, PhD in Dermatology on VEGF- the subject of the big announcement above regarding the new discovery about its effect on hair density.
Vascular Endothelial Growth Factor (VEGF) is a naturally produced chemical called a cytokine. Cytokines are a signaling mechanisms that cells use to communicate with each other. Cells with appropriate cytokine receptors react in specific ways when they receive a signal. As its name suggests, VEGF stimulates endothelial cells of blood vessels to proliferate and grow, a mechanism celled angiogenesis (angio=blood vessel, genesis=formation).
VEGF was originally identified in tumor biology. Tumors grow very large very rapidly and to do this they need a lot of nutrients. To ensure a good supply, tumor cells may produce VEGF to induce blood vessels in surrounding healthy tissue to grow into the tumor. VEGF production and increased angiogenesis can also bee seen in wound healing and in some diseases such as psoriasis. However, VEGF is also produced by normal, healthy cells in various organs to maintain a good blood supply.
VEGF as a hair growth stimulant is not a new idea. Several studies looking at product expression have demonstrated VEGF production in various hair follicle compartments. Hair follicles have a cycle of growth, called anagen and rest, telogen.
When hair follicles are resting they are relatively small and inactive, but when they enter a growth phase they become much larger and the cells of growing hair follicles are the fastest proliferating non-tumor cells in the body.
To enable this increased cellular activity, a good nutrient supply is required and it has been shown that as hair follicles leave telogen and enter anagen, angiogenesis is stimulated. An intricate network of blood vessels forms and surrounds hair follicles as they enter anagen.
This study is a significant step in our understanding of hair cycle control and is the first to perform functional assays on hair follicle growth under the influence of VEGF. The scientists were previously involved with examining VEGF and angiogenesis in skin tumors and other inflammatory skin diseases.
For their studies, they produced a genetically mutated (transgenic) mouse that consistently over expresses VEGF in the skin. In their previous studies they noted that the skin developed a very extensive system of blood vessels and they hypothesized that this might affect hair follicle activity.
This study examined tissues from the transgenic high VEGF expressing mice for the extent of angiogenesis around hair follicles, measured the size of the hair follicles, and compared these statistics with those from normal mice. In addition, the researchers injected an antibody that blocks VEGF activity into normal mice and also exposed cultured hair follicle cells to VEGF.
They found that the transgenic mice had significantly larger anagen hair follicles in association with VEGF production and angiogenesis as compared to normal mice. Blocking VEGF activity resulted in a delay of hair follicles switching from telogen to anagen and much smaller anagen hair follicles developed.
Their culture studies showed that VEGF had no direct stimulatory effect on hair follicle growth. That is, it was the formation of blood vessels that allowed increased hair follicle activity in the mutated mice and not any direct effect on the hair follicle cells by the VEGF signal.
The study concludes that VEGF has an important role in controlling hair biology and that hair follicle size is partly dependent on VEGF induced angiogenesis.
Previously it has been suggested that impaired angiogenesis may play a role in androgenetic alopecia.
However, while VEGF seems to have a significant indirect effect on hair follicles, it does not act in isolation. Many cytokines and other factors can stimulate or inhibit hair follicle activity.
Whether hair follicle growth could be stimulated by injecting VEGF or the DNA coding for VEGF into skin remains to be seen. There are potential side effect risks as the angiogenesis would not be restricted to the hair follicles. There will also be other limiting factors involved including the natural production in normal skin of angiogenesis inhibiting factors.
The maximum possible size of a hair follicle is probably limited by the size of the dermal papilla and an upper limit to the level of activity by these cells. Most likely then, gene therapy for hair loss could involve VEGF, but in itself this may not be enough.
A cocktail of DNA coding for several genes is probably required.
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