Research published earlier this year sheds light on a fundamental process which drives cell growth and death among epithelial tissues such as gut lining and skin . A disruption to the processes governing the growth and death of cells is at the root of tumor formation and health conditions associated with inflammation. Researchers led by Dr. Jody Rosenblatt at the Huntsman Cancer Institute at the University of Utah in Salt Lake City believe this new insight will help elucidate the underlying mechanisms of tumor growth.
A Balancing Act
Epithelial cells can be found throughout our bodies in organs, our digestive tract, and skin. These types of cells form a protective barrier to safeguard against pathogens like bacteria. The density of this lining is determined by the amount of cells found there, which is controlled by cellular signaling process to control the creation of new cells or the removal of existing ones. An imbalance in this process—in either direction—can cause the disruption of normal biological function. An example of too few cells can be seen in conditions such as leaky gut syndrome, where holes in the epithelial lining of the intestines allow undigested food particles into the blood stream. An example of too many cells can be seen in the growth of tumors. Dr. Rosenblatt and her team discovered the underlying system our bodies use to regulate and maintain this balance is a mechanical one that detects stretching and overcrowding of cells.
Stretching to Accommodate
This research showed that epithelial cells detect changes in density by producing signals in response to stretches and contractions. When there are too few cells their walls are stretched, signaling new cell formation. When the cells are overcrowded, their walls are compressed and signal cell death. Essentially, this process of cell density regulation is a process of tension detection. There’s a sheer elegance of this process—as with many systems of balance—and it turns out the thresholds at which these signals initiate are tightly established. Dr. Roseblatt’s team found that an increase of pressure of 1.6 times (~Phi for those paying attention) was the point at which cell death was triggered. Dr. Rosenblatt describes this process as such:
“What we found boils down to really simple principles. It’s all mechanical tension. If the cells get too crowded – 1.6-fold more crowded – then they pop some cells out that later die. The extrusion of cells enables the cell sheets to return to densities they like.”
“If the cells become too sparse, then they activate cells to divide – and that signal to divide comes from mechanical stretch. To test this, we stretched cells and found that stretch could trigger cells to divide within only one hour! The process also showed us that stretch is a normal trigger for cell division.”
Dr. Rosenblatt’s team found this process is regulated, at least partially, by the protein Piezo1. This protein along with its close relative Piezo2 are thought to be integral to the unique cation channels used for the detection of mechanical pressures in our bodies—such as sound or touch. Exactly how these proteins function or underlying cellular processes for the detection of pressures, is still largely unknown. Animal studies have shown that Piezo1 to induce cellular current in response to pressure . This makes a strong case for the role of Piezo-class proteins as being integral for cellular responses to mechanical pressure. Dr. Rosenblatt’s work seems to back up this notion, and casts valuable insight onto the underlying process of tumor formation.
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