"In recent years, researchers have gained a better understanding of the molecular machinery of cell migration, but not what directs it to happen in the first place," said lead researcher Kin Wong from the University of Arizona (UA).

The answer, it turned out, involves delicate interactions between biomechanical stress, or force, which living cells exert on one another, and biochemical signaling.

The researchers discovered that when mechanical force disappears, for example at a wound site where cells have been destroyed, leaving empty, cell-free space - a protein molecule, known as DII4, coordinates nearby cells to migrate to a wound site and collectively cover it with new tissue. This elaborate auto-regulatory system remains activated until new tissue has covered a wound.

"The results significantly increase our understanding of how tissue regeneration is regulated and advance our ability to guide these processes," Wong said.

The results represent a major advancement for regenerative medicine, in which biomedical engineers manipulate cells' form and function to create new tissues, and even organs, to repair, restore or replace those damaged by injury or disease. The same migration processes for wound healing and tissue development also apply to cancer spreading, the researchers noted.

"Knowing the genetic makeup of leader cells and understanding their formation and behaviour gives us the ability to alter cell migration," Wong added.

With this new knowledge, researchers can re-create, at the cellular and molecular levels, the chain of events that brings about the formation of human tissue. Bioengineers now have the information they need to direct normal cells to heal damaged tissue, or prevent cancer cells from invading healthy tissue.

The findings were published in Nature Communications.

 

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