(Philadelphia, PA) A team of scientists from Temple University School of Medicine and the University of Pennsylvania has moved another step closer to solving a decades-long mystery of how the all-important flow of calcium into the cell's power source, the mitochondria, is controlled.
By painstakingly shutting down the activity of 50 genes, one at a time, they have identified a protein, MCUR1, which hugs the inside of the mitochondrial membrane and is part of an elaborate mitochondrial channel pore system. MCUR1 acts as an accelerator to help regulate calcium coming into the mitochondria from the cell's large reservoir.
The results, appearing November 25, 2012 in an advance online issue of the journal Nature Cell Biology, may also point to new treatment opportunities. Understanding how to manipulate MCUR1 may help in the development of treatments for disease conditions involving excessive calcium in the cell, such as cardiovascular disease and stroke.
"Calcium is a key to regulate many fundamental processes in cells," said co-senior author Muniswamy Madesh, PhD, Assistant Professor of Biochemistry at Temple University School of Medicine and a member of Temple's Center for Translational Medicine. "Excessive calcium in the cell's mitochondria could lead to heart and neuronal mitochondrial dysfunction and cell death. This pathway could be contributing to disease conditions during ischemia/reperfusion injury and stroke, and this discovery opens up possible therapeutic interventions."
Maintaining calcium at an appropriate level is crucial for cells to work properly, and especially important in the mitochondria. Cells rely on mitochondria to generate usable energy in the form of the chemical ATP, which is necessary to carry out normal cellular and metabolic activities. ATP production in turn depends on calcium more specifically, charged calcium ions that can enter into the mitochondria from the cell's vast supply in the
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Temple University Health System