|Alan Trounson, CIRM President|
The first two articles featured in this month’s report focus on an avenue of discovery that is going to be increasingly important to regenerative medicine. They found ways to make the body’s own cells better at repairing or replacing damaged tissue, rather than transplanting replacement cells. One used a gene therapy type approach to redirect adult cells from their usual function and one used a small molecule to get an animal’s endogenous, or own, stem cells to become the needed tissue. And both documented some degree of repair.
The first project came from CIRM funded work at the Gladstone Institutes. It builds on work from the same team last year that used three genetic factors to reprogram cardiac fibroblasts, the supporting tissue in the heart, and convert them into cardiac myocytes, beating heart muscle. But that experiment was in a lab dish. In the current work the team injected the same three factors directly into the hearts of mice, in which they had induced heart attack-like lesions. About 10 to 15 percent of the fibroblasts, which normally contribute to forming scar tissue after a heart attack, converted to muscle and did improve heart function. The study was written about in more detail in an earlier blog by my colleague Amy Adams.
The second study also had CIRM funding this time at Scripps. The San Diego team worked with two mouse models of osteoarthritis. They used a high throughput screening technique to find a molecule that could direct mesenchymal stem cells to become cartilage. Out of 22,000 compounds screened, they found one that did the job. They injected it into the joints of mice once a week for four weeks and were able to detect new cartilage growth and improved movement by the animals. They seem to have succeeded in summonsing the animal's own stem cells to the site and to become the correct tissue—a potentially much less expensive repair than cell transplantation.
My full report is available online, along with links to my reports from previous months.