"From the previous work it could have seemed that GD11 was heart specific," said Wagers, "but this shows that it is active in multiple organs and cell types Prior studies of skeletal muscle and the parabiotic effect really focused on regenerative biology. Muscle was damaged and assayed on how well it could recover," Wagers explained.
She continued: "The additional piece is that while prior studies of young blood factors have shown that we achieve restoration of muscle stem cell function and they repair the muscle better, in this study, we also saw repair of DNA damage associated with aging, and we got it in association with recovery of function, and we saw improvements in unmanipulated muscle. Based on other studies, we think that the accumulation DNA damage in muscle stem cells might be reflect an inability of the cells to properly differentiate to make mature muscle cells, which is needed for adequate muscle repair.
Wagers noted that there is still a great deal to be learned about the mechanics of aging in muscle, and its repair. "I don't think we fully understand how this happening or why. We might say that the damage is modification to the genetic material; the genome does have breaks in it. But whether it's damaging, or a necessary part of repair, we don't know yet."
Rubin, whose primary research focus is on developing treatment for neurodegenerative diseases, particularly in children, said that that when his group began its GDF11 experiments, "we knew that in the old mouse things were bad in the brain, there is a reduced amount of neurogenesis (the development of neurons), and it's well known that cognition goes down. It wasn't obvious to me that those things that can be repaired in peripheral tissue could be fixed in the brain."
Rubin said that post doctoral fellow Lida Katsimpardi, the lead author on his group's paper, was taught the parabiotic experimental technique by Wagers, but conducted the Rubin grou
|Contact: B. D. Colen|