New strain of mice opening pathways for treating osteoporosis
Lincoln Potter, Ph.D., and colleagues created a breed of mice with longer, stronger and thicker bones.
But, the University of Minnesota professor needed to understand the importance of this strain of mice and its potential application in ongoing research to improve human care.
At the University of Minnesota, Dr. Potter has expertise in developing mouse models. Mayo Clinic has expertise in translating basic science into the next step of clinical research.
Dr. Potter turned to Sundeep Khosla, M.D., whose expertise in bone biology could help piece together this puzzle.
“Having a person like Sundeep is great because he knows a huge amount about bone biology, in general, and he actually sees patients so he’s just got this breadth of understanding about this project that I would never have so it’s great for me to collaborate with him,” Dr. Potter says.
In their collaboration, Drs. Khosla and Potter determined that these mice could shed light on treatment options for osteoporosis, which causes bones to become weak, brittle, and easy to fracture when the loss of old bone becomes more rapid than the replacement of new bone.
“I think the complexity of science has gotten such that, pretty much everybody is involved in what we refer to now as team science,” Dr. Khosla says.
The two were awarded funding from the Minnesota Partnership for Biotechnology and Medical Genomics in 2018 and are working on publishing a paper on their findings to open up a pathway on understanding and treating osteoporosis.
“[Grants are] very competitive, and I think it forces you to think outside of your own expertise because you need to come up with novel ideas and for that you need people with many different types of expertise and perspectives,” Dr. Khosla says.
Dr. Potter wanted to apply the discovery that he and his group made in a previous collaboration with Dr. Laurinda Jaffe’s group at the University of Connecticut Health Center involving a novel breed of mice that have longer, stronger bones, and whether the enzyme that is activated in the mutant mice can be targeted to treat osteoporosis. Dr. Potter and colleagues used knock-in technology, a type of genetic engineering, where the wild type gene is replaced with the mutant gene, to make the mice.
After designing a more active form of the enzyme, guanylyl cyclase-B, and replacing the wild type gene with the gene encoding the more active enzyme in the mouse genome, the resulting mice not only had longer bones, but they also had more bone mass. This increase in trabecular bone had more mineralization and therefore is stronger.
Dr. Potter says, “We’re into a new area and we might be able to use this pathway to treat osteoporosis or perhaps reduce the time a fractured bone takes to heal.”
The two are looking to apply for another grant to further their research.
- Maria Ly