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UCLA stem cell researchers uncover mechanism that regulates human pluripotent stem cell metabolism
Date:11/15/2011

nhibiting the stem cell's ability to respire as a method for generating energy.

As pluripotent stem cells were driven to develop into mature cell types, UCP2 expression was shut off, allowing respiration substrates to enter the mitochondria for energy generation, switching the cells from glycolysis to oxidative phosphorylation. Manipulating UCP2 expression, by keeping it switched on in differentiating cells, disturbed their maturation, a finding that could make them unsuitable for clinical use and also pointing to the importance of properly functioning metabolism for generating safe, high quality cells.

Teitell and his team confirmed these findings in both human embryonic stem cells and in induced pluripotent stem cells, which are mature body cells that are genetically reprogrammed to have similar abilities and attributes as the pluripotent embryonic stem cells.

"A main question that evolved during the study was whether it was the process of pluripotent stem cell differentiation that was altering the pattern of metabolism, or was it the change in the pattern of metabolism that altered the process of differentiation, a typical chicken-or-the-egg question," Teitell said. "We over-expressed UCP2 in the stem cells and showed that metabolism patterns changed before markers of pluripotency or cell maturation changed, indicating that changes in metabolism affect changes in differentiation and not the other way around, at least for UCP2. This was important, to show causation for metabolic changes in driving the process of cell differentiation. However, it still leaves open the key question of exactly how manipulating cell metabolism controls cell differentiation, a question we are working hard to address."

Since metabolism in pluripotent stem cells and cancer cells appear quite similar, Teitell said the finding could potentially be used to target UCP2 in malignant tumors that express it, of which there are many. Silencing UCP2 could force
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Contact: Kim Irwin
kirwin@mednet.ucla.edu
310-206-2805
University of California - Los Angeles Health Sciences
Source:Eurekalert

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