factor protein promotes thicker hair
Scientists in Boston, USA, claimed they have found a protein
normally associated with blood vessel growth that also makes
bigger. Dr. Michael Detmar, associate professor of dermatology
at Massachusetts General Hospital in Boston, who led the study
two groups of mice one "wild-type" and the other genetically
bred to produce extra vascular endothelial growth factor (VEGF)
in the skin.
The scientists found, the mice with extra VEGF grew fur faster
and thicker in the first two weeks of life. When the mice were shaved
at two months of age, they grew back fur that was 70 percent thicker
than "wild-type" mice. Blood vessels surrounding their
fur follicles were also larger and when they treated normal mice
with a drug that blocks VEGF, their fur grew in thin and developed
bald spots. "So by modulating VEGF production in the skin,
we can directly influence the size of the hair," Detmar said.
"In male pattern hair loss, it's not that the follicles are
gone. They're just miniaturized" said Detmar. "If anyone
could find a way to make the follicles bigger, men might grow hair
again." The key, he and colleagues report in the Feb. 19 issue
of the Journal of Clinical Investigation, might be a protein called
VEGF now used experimentally to help people grow their own heart
VEGF, or vascular endothelial growth factor, helps the body grow
blood vessels. It can help heart disease patients and is one of
the proteins blocked in certain experimental anti-cancer therapies
aimed at starving out tumors. The researchers are now working on
a way to get VEGF into the scalp in a cream or ointment. "The
question now is can we, by this method, improve hair growth in humans?"
said Detmar. "Applying it to humans will be a big challenge."
Vascular Endothelial Growth Factor (VEGF) is a naturally produced
chemical called a cytokine. Cytokines are a signalling mechanisms
that cells use to communicate with each other. cells with approriate
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 stimulator of hair growth is not a new idea. Several
studies looking at product expression have demonstrated VEGF production
in various hair follicle compartments. Hair folicles have a cycle
of growth, called anagen and rest, telogen. When hair follicles
are resting they are relatively small an 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 hypothesised 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 controling hair biology
and that hair follicle size is partly dependant on VEGF induced
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.