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Newly Discovered Protein Critical to Hematopoietic Stem Cell Function and Blood Formation

First Posted: Feb 02, 2014 11:23 PM EST
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A recent study examines a protein that's critical to hematopoietic stem cell function and blood formation. Researchers from the University of California believe the study of this cell function could help provide target treatments for leukemia.

According to background information from the study, hematopoietic stem cells give rise to other blood cells. Fortunately, the discovery of this protein called Lis1 helps to regulate asymmetric division of hematopoietic stem cells bysupplying them with new, adequate blood cells.

However, asymmetric division occurs when a stem cell unevenly divides into two daughter cells: one that is permanently a specialized cell, while the other remains undifferentiated and capable of further divisions, which can create health issues.

"This process is very important for the proper generation of all the cells needed for the development and function of many normal tissues," said principal investigator Tannishtha Reya, PhD, professor in the Department of Pharmacology, via a press release. For instance, when the cells divide, the Lis1 protein controls the orientation of the mitotic spindle that helps to segregate chromosomes during cell division.

"During division, the spindle is attached to a particular point on the cell membrane, which also determines the axis along which the cell will divide," Reya added, via the release. "Because proteins are not evenly distributed throughout the cell, the axis of division, in turn, determines the types and amounts of proteins that get distributed to each daughter cell. By analogy, imagine the difference between cutting the Earth along the equator versus halving it longitudinally. In each case, the countries that wind up in the two halves are different."

Yet when researchers took away the protein from the mouse model's hematopoietic stem cells, the asymmetric division increased and accelerated differentiation-thus resulting in an oversupply of specialized cells that caused the mouse to lose blood.

"What we found was that a large part of the defect in blood formation was due to a failure of stem cells to expand," said Reya. "Instead of undergoing symmetric divisions to generate two stem cell daughters, they predominantly underwent asymmetric division to generate more specialized cells. As a result, the mice were unable to generate enough stem cells to sustain blood cell production."

Next in the study, scientists studied how the cancer stem cells in mice worked after the Lis1 signaling pathway was blocked. They found that the cells lost the ability to renew themselves.  "In this sense, the effect Lis1 has on leukemic self-renewal parallels its role in normal stem cell self-renewal," Reya said.

More information regarding the study can be found via the journal Nature Genetics

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