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Calcium-mediated effect plays key role in cell disposal, researchers discover

A research team from Kyushu University in Japan has recently discovered a calcium-based mechanism that plays a key role in the disposal of dead cells, shedding light on how our bodies protect themselves from injury and disease. In their study, published in Current Biology, the team unveiled how calcium ion levels are essential for the efficient removal of dying or apoptotic cells from epithelial tissues (cells lining the body surface), using genetically engineered epithelial tissue cultures, molecular markers, and advanced imaging techniques.

The surfaces of our bodies, including the skin and internal organs, are covered by sheets of epithelial cells that act as vital barriers. When these cells become damaged and die (apoptosis), neighboring cells quickly band together to push them out and seal any gaps through which foreign substances could enter and potentially lead to infections or inflammation. Although this complex process is essential for maintaining a healthy epithelial barrier, the exact mechanism underlying it has not been entirely clear—until now.

The study, led by Professor Junichi Ikenouchi and his colleagues, Dr. Kenji Matsuzawa and Mr. Yuma Cho, the first author, from Kyushu University, also included contributions from collaborators from the University of Tokyo and Health Sciences University of Hokkaido in Japan.

To begin with, the team induced apoptosis in individual epithelial cells using a focused laser and observed the response in the surrounding cells. They then observed how nearby cells reacted by modifying them to express special calcium ion probes called GCaMP6, which allowed them to visualize real-time calcium changes.

Interestingly, they found that the neighbors of the apoptotic cell showed a significant spike in calcium levels, particularly near the membrane regions interfacing with the dying cell. The researchers named this intriguing phenomenon the "calcium response in effectors of apical extrusion (CaRE)."

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