s took this a step further and studied actual mice that lacked the autophagy genes in their lung and retinal tissues, finding that healthy cells engulfed fewer than 25 percent of dead cells during embryonic development, compared to 75 percent in normal mice.
“Without autophagy, the dead cells just don’t get engulfed very efficiently,” Dr. Levine said. “If you don’t have rapid removal of dead cells, you get a lot of unwanted inflammation.”
But why do the dead cells in normal embryos disappear?
Through the study, Dr. Levine and the researchers demonstrated it is due to autophagy’s ability in dying cells to prompt signals for engulfment by healthy cells. Engulfment depends on signals from the dying cells. An “eat me” signal is made when the chemical phosphatidylserine is exposed on the outside of cell’s membrane. A “come get me” signal is made through the secretion of another chemical, lysophosphatidylcholine.
The autophagy-deficient mouse embryonic bodies failed to develop normally because their cells didn’t expose phosphatidylserine and secreted low levels of lysophosphatidylcholine, the study shows.
“In other words, they didn’t generate either of these two needed signals,” Dr. Levine said.
The researchers also found that the cells of the autophagy-deficient mouse embryos had low levels of ATP, a vital energy source for many cellular functions. Autophagy is known to generate amino and fatty acids utilized in ATP production.
Treatment with an alternative fuel, methylpyruvate, restored normal levels of ATP in autophagy-deficient mouse embryonic bodies and bypassed the bodies’ failure to prompt signals needed for the healthy cells to engulf the dead ones, Dr. Levine said.
“This study shows that autophagy-induced signals are essential for normal development,” she said. “It also raises the possibility that defects in autophagy might spur inflammation in human conditions with cePage: 1 2 3 Related medicine news :1
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