CCC 2011: Repair for Damaged Tissue

December 5, 2011

With the recent understanding that progenitor cells in the adult body can help heal a damaged heart, both by repairing heart muscle tissue and building new blood vessels to supply oxygen, researchers have been looking for ways to help these cells work harder and live longer.

Dr. Darryl Davis, an electrophysiologist and regenerative medicine researcher at the Heart Institute, discussed a set of molecular markers that differentiate cardiac progenitor cells (CPCs) from other cell types. CPCs are not abundant in the native heart: using its panel of markers, Dr. Davis’ group identified only a fraction of 1 per cent of cells in samples from adult mouse hearts as CPCs.

With the group’s cell expansion techniques, it was able to produce large cultures containing 10 per cent CPCs. This increased the number of cells collected from about 3,000 to about 130,000—a substantial number when looking at the potential of injecting CPCs into a damaged heart to stimulate repair.

Nicholas Latham, a graduate student working with Dr. Davis, presented results from research testing the regenerative capacity of human endothelial progenitor cells (EPCs) in the heart. EPCs help build the blood vessels that feed the heart.

They found that while EPCs produced a more extensive profile of signalling proteins that draw other molecules involved in tissue repair to the heart, EPCs and CPCs appeared to have similar capacities to promote the growth of blood vessels in cell culture. Latham concluded that a combination cell therapy may have synergistic effects and enhance cardiac stem-cell therapy in future experiments.

Ali Ahmadi, from Erik Suuronen’s laboratory, presented research into whether a supportive collagen matrix can increase the retention and survival of transplanted CPCs. Currently, when CPCs are transplanted into the adult heart, only 1 to 10 per cent survive. The researchers saw improved survival of CPCs, improved heart function, and improved blood flow with the collagen matrix—and signalling by a protein that can protect CPCs (integrin-linked kinase) was significantly higher.

Joanne McBane, also in the Suuronen laboratory, presented data showing that a collagen-chitosan matrix, under development to support islet transplantation for diabetes treatment, helps the formation of new blood vessels for transplanted islets and therefore should improve cell survival. The collagen-chitosan matrix also provided a reduction over time in signalling molecules that could encourage the body to attack the transplanted islets, while it allowed for an increase in signalling molecules that could help protect the islets.