Growth Factor Responsible for Triggering Hair Follicle Generation During Wound Healin

[squeegee]

News Release
June 2, 2013
[h=1]Growth Factor Responsible for Triggering Hair Follicle Generation During Wound Healing Identified, Found in Cells of Short Supply in Humans[/h] [h=2]Penn Medicine Study Highlights Interplay between Immune System and Tissue Regeneration[/h]
PHILADELPHIA - Researchers in the Perelman School of Medicine at the University of Pennsylvaniahave determined the role of a key growth factor, found in skin cells of limited quantities in humans, which helps hair follicles form and regenerate during the wound healing process. When this growth factor, called Fgf9, was overexpressed in a mouse model, there was a two- to three-fold increase in the number of new hair follicles produced. Researchers believe that this growth factor could be used therapeutically for people with various hair and scalp disorders. The study appears in an advance online publication of Nature

http://www.uphs.upenn.edu/news/News...Feed:+penn-medicine-news+(Penn+Medicine+News)

 

[Donc83]

So how could this help? Cotsarelis has been making discoveries for 10 years and nothing has come of it. Im sick of false hope from these scientist with thick heads of hair.

 

[Jacob]

Good find. That reminds me(to Donc83 as well) of this story http://www.cbsnews.com/8301-204_162...ne-day-eliminate-need-for-insulin-injections/ ...which reminds me that it's insane for anyone to say they know exactly what causes what and what is the "cure" etc etc. It's all so damn complicated.

 

[IDW2BB]

Why couldn't a bald dude with a sunburn rub some fgf9 topical on his head and see results?

 

[Boomer01]

People have long been waiting for a valid breakthrough on baldness, and now Penn University has studied a new Growth Factor (protein-Fgf9) that is showing promise. The scientists examined wounds and scars, where hair is known not to regrow. They questioned why an adult person has blocked hair follicle growth upon wound-healing while mice do not? It appears that adult mice have the ability to create more Fgf9 versus adult humans. When scientist reduced the Fgf9 response in mice, their hair regrowth in wounds was in fact inhibited.

Could the next step be treatments intended to compensate for the lack of Fgf9 to benefit hair regrowth in its entirety for humans? If studies continue perhaps baldness may be a thing of the past.

http://likes.com/misc/science-is-to...6IDExNDQ2MTcyMjUsICJwb3N0X2lkIjogMjUxNDQ3NTV9

 

[IDW2BB]

Posting two studies for review (sorry!)opsblush:http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3302445/

Canonical Wnt signaling plays an important role in embryonic and postnatal blood vessel development. We previously reported that the chromatin-remodeling enzyme BRG1 promotes vascular Wnt signaling. Vascular deletion of Brg1 results in aberrant yolk sac blood vessel morphology, which is rescued by pharmacological stimulation of Wnt signaling with lithium chloride (LiCl). We have now generated embryos lacking the chromatin-remodeling enzyme Chd4 in vascular endothelial cells. Unlike Brg1 mutants, Chd4 mutant embryos had normal yolk sac vascular morphology. However, concomitant deletion of Chd4 and Brg1 rescued vascular abnormalities seen in Brg1 mutant yolk sacs to the same extent as LiCl treatment. We hypothesized that Wnt signaling was upregulated in Chd4 mutant yolk sac vasculature. Indeed, we found that Chd4 deletion resulted in upregulation of the Wnt-responsive transcription factor Tcf7 and an increase in Wnt target gene expression in endothelial cells. Furthermore, we identified one Wnt target gene, Pitx2, that was downregulated in Brg1 mutant endothelial cells but was rescued following LiCl treatment and in Brg1 Chd4 double mutant vasculature, suggesting that PITX2 helps to mediate the restoration of yolk sac vascular remodeling under both conditions. We conclude that BRG1 and CHD4 antagonistically modulate Wnt signaling in developing yolk sac vessels to mediate normal vascular remodeling.

http://www.ncbi.nlm.nih.gov/pubmed/23602386

Hair follicle stem cells (bulge cells) are essential for hair regeneration and early epidermal repair after wounding. Here we show that Brg1, a key enzyme in the chromatin-remodeling machinery, is dynamically expressed in bulge cells to control tissue regeneration and repair. In mice, sonic hedgehog (Shh) signals Gli to activate Brg1 in bulge cells to begin hair regeneration, whereas Brg1 recruits NF-κB to activate Shh in matrix cells to sustain hair growth. Such reciprocal Brg1-Shh interaction is essential for hair regeneration. Moreover, Brg1 is indispensable for maintaining the bulge cell reservoir. Without Brg1, bulge cells are depleted over time, partly through the ectopic expression of the cell-cycle inhibitor p27(Kip1). Also, bulge Brg1 is activated by skin injury to facilitate early epidermal repair. Our studies demonstrate a molecular circuit that integrates chromatin remodeling (Brg1), transcriptional regulation (NF-κB, Gli), and intercellular signaling (Shh) to control bulge stem cells during tissue regeneration.

 

[uncomfortable man]

Hey lets just have them turn people into mice amirite? That way hair loss treatments can finally work on us and it would probably be easier for them than I don't know CLONING HAIR FOLLICLES! derp.