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Temple-Penn researchers identify calcium 'accelerator' to keep cell power supply going
Date:11/25/2012

, and its activity level increases when the extra-mitochondrial calcium levels increase. When there is a high calcium level, say during a disease state, the MCUR1 senses this and facilitates the channel activity, dumping calcium inside," Dr. Madesh explained.

Calcium Control as a Targeted Therapeutic

Dr. Madesh explained that in some disease conditions such as ischemic reperfusion injury (tissue damage that occurs when blood returns to tissue after a period without oxygen), stroke involving brain injury from ischemia, and myocardial infarction calcium floods into the mitochondria. "The mitochondria have a massive membrane potential and grab external calcium. The mitochondria then are overloaded and rupture, leading to cell death and possible organ injury."

Because some diseases are characterized by an overabundance of calcium in the mitochondria, a possible therapy could involve slowing down the amount of calcium coming into the mitochondria. "We want to control the calcium entering the mitochondria," he said.

"Further studies already underway should reveal the precise molecular mechanisms by which MCUR1 accelerates the channel pore MCU, providing insights into mitochondrial bioenergetics," said first author Karthik Mallilankaraman, PhD, a postdoctoral fellow in the Department of Biochemistry and the Center for Translational Medicine at Temple University School of Medicine.


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Contact: Steven Benowitz
steven.benowitz@tuhs.temple.edu
215-707-4784
Temple University Health System
Source:Eurekalert

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