Translational Medicine
Jul
30
A super-active form of Vitamin D boosts the capacity of stem cells to enhance and maintain their ability to induce hair growth, a team of Japanese researchers concluded in a study that could someday lead to a cell therapy for human baldness.
In research results published in STEM CELLS Translational Medicine, researchers from the University of Tokyo (UT) School of Medicine, Osaka University, and the Japan Science and Technology Agency found that treating dermal papilla cells (DPCs) with VD3 significantly enhanced the growth of new hair over that of the control group.
“We also observed a better rate of maturation of the follicles. In other words, the hair grew thicker and lasted longer,” Noriyuki Aoi, M.D., of UT’s School of Medicine said in a statement.
Dr. Aoi and UT’s Kotaro Yoshimura, M.D., led the team in building upon previous studies that have demonstrated how DPCs can stimulate epithelial stem cells to become hair by increasing their transforming growth factor TGF-ß2 and alkali-phosphatase activity. The team collected DPCs from volunteers who had undergone facelifts, incubated the DPCs with VD3 and then grafted them onto hairless skin samples taken from rats.
“The results suggest that (VD3) may be useful in expanding human DPCs with good quality, and help establish a DPC transplantation therapy for growing hair,” Dr. Yoshimura said in the statement.
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Journal for Translational Medicine
Translational Medicine
Jul
30
A team of researchers in Japan has discovered that VD3, a super-active form of Vitamin D, boosts stem cells to enhance and maintain their ability to induce hair growth. This new study, reported in STEM CELLS Translational Medicine, builds upon previous studies that have demonstrated how dermal papilla cells (DPCs) can stimulate epithelial stem cells to become hair.
“We had already discovered how VD3 increases the transforming growth factor TGF-ß2 and alkali-phosphatase activity — two essential features of hair-inducing DPCs. This time we focused on VD3’s therapeutic potency and values for hair regeneration,” said Kotaro Yoshimura, M.D. “The results suggest that it may be useful in expanding human DPCs with good quality, and help establish a DPC transplantation therapy for growing hair.”
Yoshimura and Noriyuki Aoi, M.D., both of the University of Tokyo (UT) School of Medicine, led scientists from UT, Osaka University and the Japan Science and Technology Agency in the investigation. After running more tests on how VD3 affected another crucial element for hair growth called Wnt10b gene expression, they collected DPCs from volunteers who had undergone facelifts, incubated the DPCs with VD3 and then grafted them onto hairless skin samples taken from rats.
“We found that treating the dermal papilla cells with VD3 significantly enhanced the growth of new hair over that of the control group,” Dr. Aoi said. “We also observed a better rate of maturation of the follicles. In other words, the hair grew thicker and lasted longer.”
“This study may contribute to the development of a cell-based therapy for hair regeneration,” said Anthony Atala, MD, Editor of STEM CELLS Translational Medicine and director of the Wake Forest Institute for Regenerative Medicine. “The research team shows the potential impact of vitamin D to boost the capacity of certain cells in the skin to form hair.”
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Journal for Translational Medicine
Translational Medicine
Jul
26
Rapamycin, an immunosuppressant drug used in a variety of disease indications and under study in aging research labs around the world, improved function and extended survival in mice suffering from a genetic mutation which leads to dilated cardiomyopathy (DCM) and rare muscular dystrophies in humans. There are currently no effective treatment for the diseases, which include Emery-Dreifuss Muscular Dystrophy and Limb-Girdle Muscular Dystrophy. The familial form of DCM often leads to sudden heart failure and death when those affected reach their 40′s and 50′s.
In research published in the July 25, 2012 online edition of Science Translational Medicine, scientists from the Buck Institute and other organizations focused on mutations in the gene LMNA, which produces A-type lamins. Mutations in this gene are associated with at least 13 diseases, with DCM among the most common. DCM accounts for 60 percent of all cardiomyopathy cases. LMNA mutations may account for up to one-third of patients that are diagnosed as having DCM and conduction disease. DCM causes a thinning of the left ventricle and loss of cardiac function. The study showed that deletion of the LMNA gene led to ramped up activity in the molecular pathway mTOR (mammalian target of rapamycin) and that treatment with rapamycin turns down the abnormal signaling. Senior author Brian K. Kennedy, PhD, President and CEO of the Buck Institute for Research on Aging, says treatment with rapamycin extended mouse lifespan by 60 percent in a relatively rapid onset model of disease. “What’s particularly exciting is that this work offers a therapeutic possibility where there has been none,” said Kennedy. “This study, along with others, suggests that clinical trials of rapamycin and its derivatives be initiated for human patients suffering from this form of DCM.” Rapamycin has been shown to extend healthspan in normal mice. It and the mTOR pathway are being intensively studied in aging research laboratories around the world. Kennedy, who came to the Buck Institute from the University of Washington where much of this work was done, said the study first focused on rapamycin in a mouse model of Hutchinson-Gilford Progeria Syndrome, a premature aging disorder that is also based on a mutation in lamin-A. “We found to our surprise that rapamycin is beneficial for DCM instead,” he said. “As we investigate and understand the cellular pathways that get disrupted or altered with aging, we will likely be putting our hands on common pathways that become disregulated in various disease states,” said Kennedy. “This started out as a study about aging, and it’s pointed us toward a specific disease indication, where we might be able to generate a new therapeutic. I am hoping this is the first of many times that this happens.”
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Journal for Translational Medicine
