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Tiny feet on cells can sense defects and stall migration to heal wounds

Tiny feet on cells can sense defects and stall migration to heal wounds

phys.org 17.08.2026 21:20 9 baxış
Cells travel through the body both individually and in collective groups during development, wound healing and diseases such as cancer. New research from the McKelvey School of Engineering at Washington University in St.

This article has been reviewed according to Science X's editorial process and policies. Editors have highlighted the following attributes while ensuring the content's credibility: Cells travel through the body both individually and in collective groups during development, wound healing and diseases such as cancer. New research from the McKelvey School of Engineering at Washington University in St.

Louis shows that cells can sense even the smallest defects, or micro-injuries, in the surface beneath which they travel and stall long enough to begin the healing process. Amit Pathak, professor of mechanical engineering & materials science, and members of his lab, including Hannah Zmuda, who earned a doctorate in biomedical engineering from McKelvey Engineering in 2025, found that the tiny feet on the leading edge of a group of cells can sense a defect of only a few microns in a membrane below the surface of the extracellular matrix, which supports cell growth and provides structure when tissues regenerate. Their results were published July 31, 2026, in Cell Reports.

Groups of cells travel along the extracellular matrix (ECM), which has a basement membrane, a protective layer made from collagen IV that acts as a tissue barrier for organs, and the interstitial matrix, which is made of collagen I and sits below the basement membrane. These cells move along the ECM with tiny feet called filopodia, which are so sensitive that they can detect small defects in the basement membrane and stop for up to eight hours—but only when collagen IV was present. "The filopodia were something we specifically were not looking for, but they turned out to be the things that control this sensing of these tiny defects in extracellular surfaces," Pathak said.

Interestingly, when the filopodia sense collagen I or stiffer ECM, they kept moving over the defect, Pathak said, showing that a difference in stiffness is important. "In cancer, the basement membrane gets degraded completely, so the cells have access to collagen type I, which is the more native tissue," Pathak said. "In tumor invasion, you want them to notice the gap and stop, because stalling is good in cancer.

If the cells don't notice small wounds and keep going, that means there was no healing done. If they stall and deposit new extracellular matrix, they heal the wound and then move on." Zmuda and the team also found that the environment around the cells affects how strongly the stalling spreads, particularly how stiff the surrounding material is and how osmolar the fluid medium is, in addition to the type of collagen that is present. "When we culture cells in the body, the fluid is not all the same," Pathak said.

"There are differences in salt, sugar and water, which have a huge effect on osmolality. This changes cell migration and defect sensing. The membrane changes their feet, and the filopodia change." The team conducted their research with human mammary epithelial cells, Madin-Darby canine kidney cells and primary zebrafish keratinocytes from fish scales.

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