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(Ivanhoe Newswire) There is a new HUMMR on the block. It is smaller than its automotive counterpart, but no less powerful.
Scientists at the University of Rochester Medical Center have identified a protein, which they have dubbed HUMMR (hypoxia upregulated mitochondrial movement regulator) that may shed new light on how the brain recovers from a stroke.
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The primary role of HUMMR is to regulate the proper transport and distribution of mitochondria throughout the cell, essentially ensuring that they are in the correct position. Mitochondria are cellular power plants that generate most of a cells supply of chemical energy. "Understanding the molecular machinery that helps distribute mitochondria to different parts of the cell has only recently begun to be understood," University of Rochester Medical Center neurologist David Rempe, M.D., Ph.D., the lead author of the study was quoted as saying. "We know that in some disease states that mitochondria function is modified, so understanding how their activity is modulated is important to understanding how the brain responds to a pathological state."
Understanding the mechanisms that regulate the movement of mitochondria may help scientists identify how the brain's cells ward off and potentially repair damage. An example is the role that mitochondria play as a calcium buffer. One of the mitochondria's functions is to help control the concentration of calcium in the cell. This capacity is important, particularly in instances when calcium levels in the cell spike during a stroke, a condition which contributes a cascading series of events that ultimately lead to a state called excitotoxicity and cell death.
One of the keys to identifying the function of HUMMR has been the appreciation in that the body operates at a relatively low oxygen level. While the air we breathe consists of approximately 20 percent oxygen, the cells in the brain sit at somewhere between 2 percent to 5 percent oxygen. This creates a "normal" state of hypoxia in the brain.
However, the concentration of oxygen in the brain can drop even further in instances such as a stroke, when blood flow to a portion of the brain is cut off. This decrease in oxygen promotes the expression of HUMMR which, in turn, mobilizes mitochondria. More mitochondria in the correct position may mean the cell has a greater capacity to filter out toxic levels of calcium. Rempe and his colleagues are now investigating the role that HUMMR may play in stroke models, particularly whether or not this activity helps protect vulnerable cells that lie just outside the core areas of the brain that are damaged by stroke.
SOURCE: Journal of Cell Biology, June 15, 2009
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