Researchers discovered that the E-cadherin protein complex, known for binding cells together, also enables epithelial cells to engulf and clear dead cells from tissue.
Key facts
- •The E-cadherin complex includes E-cadherin and three additional proteins that maintain structural strength in epithelial tissues.
- •Live imaging showed that epithelial cells maintain their barrier function by keeping their upper surfaces unchanged while deforming their lower surfaces to engulf debris.
- •Experiments revealed that removing a specific 'brake' protein from the complex made cells too stiff to properly clear dying cells.
- •Blocking E-cadherin in early mouse embryos resulted in dying cells remaining uncleared, suggesting the mechanism is shared among vertebrates.
- •The study was led by Verena Ruprecht and published in the journal Nature Communications.
A study published in Nature Communications reveals that the E-cadherin complex, which provides structural integrity to epithelial tissues, plays a dual role in clearing cellular debris. Led by ICREA Research Professor Verena Ruprecht, the team observed this process in zebrafish and mouse embryos. The findings suggest that epithelial cells repurpose their adhesion machinery to physically engulf dying cells, a mechanism that may be essential for preventing chronic inflammation.
Mechanism of Cellular Cleanup
The E-cadherin complex functions by connecting epithelial cells in areas such as the skin, gut, and airways. During the cleanup process, the lower surface of an epithelial cell deforms to wrap around a dying cell, while the upper surface remains stable to maintain the tissue barrier. This process requires specific proteins within the complex to act as tethers to the cell's internal skeleton, allowing for the transmission of force needed to swallow the debris.
Implications for Inflammation
The research highlights that efficient removal of dying cells depends on both chemical signaling and the physical ability of cells to reshape themselves. When dead cells are not cleared, they can rupture and release contents that contribute to chronic inflammation. While the study confirms this mechanism in zebrafish and mouse embryos, researchers are now investigating whether the same process occurs in adult tissues or human cells.
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This article was independently rewritten by ManyPress editorial AI from reporting originally published by ScienceDaily.
