Researchers at Massachusetts General Hospital (MGH) have been able to grow hair faster and thicker on mice thanks to a protein that promotes blood vessel growth in their skin. The mouse hair follicles – while no greater in number than those of normal mice – are individually bigger. Collectively, they increase the total volume of hair by 70 percent, the MGH research team reports in the Feb. 19 Journal of Clinical Investigation.
If the protein has the same powers in humans, it could lead to the first angiogenic therapy for male pattern baldness. "In male pattern hair loss, it's not that the follicles are gone. They’re just miniature follicles," says Michael Detmar, MD, associate professor of dermatology at MGH and lead author on the study. "If anyone could find a way to make the follicles bigger, men might grow hair again." The discovery that increasing blood flow to the scalp helps stave off baldness may be old news to many barbers. For years, they have been advising clients to massage their scalps as way of stimulating circulation and hair growth.
Blood Vessels Hold Key To Thicker Hair Growth
A few scientific studies have suggested that people with hair loss may have fewer blood vessels. But no one had actually measured how closely blood vessel growth is correlated with hair growth, or what might cause scalp vessels to grow in the first place.
To explore these questions, Kiichiro Yano, a research associate in dermatology at MGH, and his colleagues compared two groups of mice, one normal and one genetically programmed to produce an abundance of a protein known to trigger blood vessel growth, VEGF. The VEGF-enhanced mice grew hair faster and thicker in the first two weeks of life than did the control mice.
The VEGF-enhanced mice also regrew hair faster. Shaved 8 week-old VEGF-mice not only grew hair back sooner, they exhibited a 30 percent increase in hair follicle diameter 12 days after depilation. "By overall volume, the hair was about 70 percent thicker than in wild-type mice," says Detmar. Blood vessels located in the skin surrounding the pumped-up hair follicles were 40% larger in diameter than those found in normal mice, suggesting that the VEGF-mediated angiogenesis was causing the hair to grow faster and thicker.
When normal mice were treated with an antibody that blocks VEGF activity and then shaved, their hair grew back slower and was thinner than their untreated littermates. Twelve days after depilation, the VEGF-deprived mice still displayed bald spots and overall reduced hair growth. "So by modulating VEGF, we can directly influence the size of the hair," says Detmar.
As for how the VEGF-inspired blood vessels are plumping up the hair shafts, the researchers believe they may be delivering an extra supply of growth factors, in addition to oxygen and nutrients. Detmar and his colleagues are developing a technique to deliver VEGF topically to the scalp. "The question now is can we, by this method, improve hair growth in humans," he says. "Applying it to humans will be the big challenge."
New insights into muscle adaptation to exercise
DURHAM, N.C. -- Duke University Medical Center researchers have identified the skeletal muscle changes that occur in response to endurance exercise and have better defined the role of vascular endothelial growth factor (VEGF) in creating new blood vessels, known as angiogenesis, in the process.
VEGF is a protein known to trigger blood vessel growth by activating numerous genes involved in angiogenesis.
The researchers' new insights could provide a roadmap for medical investigators as they seek to use VEGF in treating human conditions characterized by lack of adequate blood flow, such as coronary artery disease or peripheral arterial disease.
Using mice as animal models, the researchers found that exercise initially stimulates the production of VEGF, which then leads to an increase in the number of capillaries within a specific muscle fiber type, ultimately leading to an anaerobic to aerobic change in the muscle fibers supplied by those vessels. The VEGF gene produces a protein that is known to trigger blood vessel growth.
The results of the Duke experiments were presented by cardiologist Richard Waters, M.D., Nov. 8, 2004, at the American Heart Association's annual scientific sessions in New Orleans. Walters said:
It is known that exercise can improve the symptoms of peripheral arterial disease in humans and it has been assumed that angiogenesis played a role in this improvement, however, the clinical angiogenesis trials to date utilizing VEGF have been marginally successful and largely disappointing, so we felt it would be better at this point to return to animal studies in an attempt to better understand the angiogenic process.
The Duke team performed their experiments using a mouse model of voluntary exercise. This experimental approach is important, they explained, because most skeletal muscle adaptation studies utilize electrical stimulation of the muscle, which is much less physiologic and does not as closely mimic what would be expected in human exercise.
When placed in the dark with a running wheel, mice will instinctively run, the researchers said. In the Duke experiments, 41 out of 42 mice "ran" up to seven miles each night. At regular intervals over a 28-day period, the researchers then performed detailed analysis of capillary growth and the subsequent changes in muscle fiber type and compared these findings to sedentary mice.
Mammalian muscle is generally made up of two different fiber types – slow-twitch fibers requiring oxygen to function, and the fast-twitch fibers, which function in the absence of oxygen by breaking down glucose. Because of their need for oxygen, slow-twitch fibers tend to have a higher density of capillaries. Walters said:
Exercise training is probably the most widely utilized physiological stimulus for skeletal muscle, but the mechanisms underlying the adaptations muscle fibers make in response to exercise is not well understood. What we have shown in our model is that increases in the capillary density occur before a significant change from fast-twitch to slow-twitch fiber type, and furthermore, that changes in levels of the VEGF protein occur before the increased capillary density.
Interestingly, capillary growth appears to occur preferentially among fast-twitch fibers, and it is these very fibers that likely change to slow-twitch fibers. Since exercise has the potential to impact an enormous number of clinical conditions, therapeutic manipulations intended to alter the response to exercise would benefit from a more detailed understanding of what actually happens to muscle as a result of exercise.
The exact relationship between VEGF, exercise induced angiogenesis, and muscle fiber type adaptation is still not clear and will become the focus of the group's continuing research. The findings from the current study, however, are providing important temporal and spatial clues to the adaptability process.
Note: Working the scalp muscles adequately is enough to cause oxygen deprivation in scalp tissue. This oxygen deprivation in turn stimulates angiogenesis.