Osteoarthritis researchers from the University of Southern California offer new insights on how gene activity drives the development of cartilage. This knowledge, they suggest, may help provide a repair strategy.

Based on their studies, the scientists identified and characterized unique cell populations that form the superficial zone of human joint cartilage. The zone has the most critical role in cushioning the joint and is often partially or completely lost in arthritis.

The study, from Keck School of Medicine of USC scientists in the USC Stem Cell laboratory of Denis Evseenko, and colleagues, was published recently in Nature Communications.

“Our results not only offer a unique molecular atlas of human skeletal development, but also define a strategy for joint cartilage repair,” said Evseenko, the study’s corresponding author and an associate professor of orthopedic surgery, and stem cell biology and regenerative medicine at the Keck School of Medicine, in a media release from University of Southern California.

In a series of experiments, postdoctoral scholar-research associate Gabriel Ferguson and postdoctoral scholar-research associate Ben Van Handel and colleagues compared the gene activity of developing human cartilage cells with several other cell types.

First they compared the cartilage cells to four other types of developing human cells: the precursors to bone, muscle, tendon and ligament. As the cartilage matured, the genes specific to cartilage became increasingly active, while genes related to the other cell types became repressed.

The scientists then compared these developing human cartilage cells to equivalent cells from mice. The team found many broad similarities in gene activity.

The researchers also carried out a detailed comparison of ordinary human cartilage cells and stem cell-derived human cartilage cells, taking into account genetics, genetic regulation, and function.

They demonstrated that stem cell-derived cartilage does not fully develop in the Petri dish but rather retains the genetic hallmarks typical of fetal cartilage. However, if the scientists transplanted stem cell-derived human cartilage at a particular stage of development into an arthritic rat, the cartilage would lose its fetal hallmarks and fully mature—regenerating the critical superficial zone, the release explains.

[Source(s): University of Southern California, Science Daily]