Researchers have created a synthetic “cellular glue” that can help cells bond together to different degrees. The technique could help speed up wound healing, even in tissues that don’t heal well naturally, and eventually allow scientists to build better organs.
The body is made up of trillions of cells, and to make sure skin cells stay next to skin cells and liver cells next to liver cells, they all contain tiny structures called cell adhesion molecules (CAMs). These are proteins that sit on the surface and bind to adjacent cells with varying strength, holding organs together.
Different tissues get their properties from how strong those bonds are. For instance, organs have very tight bonds to keep their form, while the immune system has weaker bonds so that cells can move around more easily. But despite their important role, CAMs are an often overlooked component when scientists are trying to engineer tissues.
So for the new study, researchers at the University of California San Francisco (UCSF) have developed synthetic cellular adhesion molecules (synCAMs). Each of the molecules contains two parts – one sits on the outside of the cell and works like a receptor, dictating which other cells it will bond with. The second part is contained inside the cell and determines the strength of each bond. When these two pieces are taken together, it allows the scientists to customize these molecules to match the wide variety of natural cell bonds.
“We were able to engineer cells in a manner that allows us to control which cells they interact with, and also to control the nature of that interaction,” said Wendell Lim, senior author of the study. “This opens the door to building novel structures like tissues and organs.”
The team says that being able to make synCAMs could be a boost to regenerative medicine, potentially helping patch up tissues that normally don’t heal on their own, such as nerves or heart tissue, or grow organs in the lab to study development, disease and drugs.
The research was published in the journal Nature.
Source: UCSF
