The genes responsible for the rapid growth of antler and hardening are identified | Information Center



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To investigate, Yang and his laboratory went to a deer farm in California, where they collected samples of early cervid tissue, mostly skeletal stem cells. The woods grow up and down; so that as they develop, a reservoir of stem cells remains at the top of the woods and continues to proliferate. At the beginning of development, the woody tissue is soft, a little like the cartilage of your nose. The sampling of cells is an easy task for Yang and safe for the male. It is only at the second stage of development that the wood will mineralize and become rigid.

Back in the lab, scientists used a variety of techniques to decipher the genetics behind wood growth, including RNA analyzes, a molecule that can be used to perform specific gene instructions, as well as studies. of "knock-down" and "overexpression" of genes. that hinder the function of the gene or return it, respectively. Comparative analyzes of RNA between antler stem cells and human bone marrow stem cells led Yang to a collection of genes that seemed to have a unique expression in the woods. From this pool, he restricted research by altering gene function and observing how different levels of gene expression affected tissue growth in mouse cells.

In the mouse cells, Yang found that when the uhrf1 gene was taken out of service, bone tissue could still grow, but not so quickly. Scientists only became aware of the rapid cell proliferation characteristic of wood growth when uhrf1 was fully functional. Similarly, when s100a10 was overexpressed, calcium deposits increased and the cells manipulated more rapidly mineralized.

"The regeneration of the woods is a unique phenomenon that, in my opinion, deserves to be studied simply out of curiosity, but hey, it could have really interesting applications for human health," Yang said.

Apply the genetics of the woods to humans

The researchers hope that their knowledge of deer antler genes could illuminate new approaches to treating diseases such as osteoporosis. In healthy bones, two types of cells – osteoblasts and osteoclasts – act as opposing forces. Osteoblasts produce new bone tissue, while osteoclasts break down old bone. Both types of cells work in a yin and yang style to continuously form and degrade bone to maintain a balanced bone structure. In osteoporosis, the function of osteoclasts exceeds osteoblasts and the bone begins to break down.

"We are only at the beginning of this research, but our ultimate goal is to determine how to apply the same underlying biology that allows for rapid bone regeneration in deer antlers to help treat conditions." human bone, such as osteoporosis, "Yang said.

Yang plans to continue research on several types of deer to confirm that uhrf1 and s100a10 slow the rapid growth of wood among species. In addition, he plans to test the functioning of genes in human cell lines, while continuing to analyze how ufh1 and s100a10 act at the molecular level, looking for possible functional pathways.

"There is a lot of work to be done, but it could be a single model of bone regeneration, and our initial work here has begun to lay the groundwork for future studies," Yang said.

The other co-authors of the article at Stanford are postdoctoral researchers Dan Wang, PhD, and Bin Zhang, PhD; Norma Neff, PhD, former director of DNA sequencing; Rashmi Sharma, former undergraduate researcher; William Maloney, MD, Professor of Boswell Orthopedic Surgery and President; and Professor of Bioengineering and Applied Physics, Stephen Quake, PhD.

Peter Yang is a member of Stanford Bio-X, Stanford Cardiovascular Institute, Stanford ChEM-H, the Stanford Children's Health Research Institute and the Stanford Neurosciences Institute.

Scientists from the Tenth People's Hospital of Tongji University, Calico Life Sciences and the Key State Laboratory for the Molecular Biology of Special Economic Animals also contributed to the study.

The research was funded by the National Institutes of Health (grants R01AR057837, R01AR057837, R01DE021468 and S10RR027431), the Ministry of Defense, the Boswell Foundation and the AO Foundation.

The Stanford Orthopedic Surgery Department also supported the work.

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