Dematin key to erythrocyte membrane stability in mice
FROM BLOOD
Dematin is newly recognized as a protein that is crucial to red blood cell (RBC) membrane integrity, and dematin’s absence in mice resulted in severe abnormalities of erythrocyte shape, membrane stability, and hemolytic anemia, Yunzhe Lu of Tufts University, Boston, and her colleagues reported in the journal Blood.
The finding indicates that dematin is the major determinant of membrane stability within the junctional protein complex.
The researchers defined the role of dematin by designing a mouse model that lacked the protein. Affected mice developed severe anemia and had abnormally shaped erythrocytes with unstable membranes.
They examined the mechanism behind erythrocyte membrane instability in the mice by using membrane protein analysis, domain mapping, electron microscopy, and dynamic deformability measurements. Although many membrane and cytoskeletal proteins remained at their normal levels, spectrin, adducin, and actin were greatly reduced in these erythrocytes. The findings indicate that dematin plays a critical role in maintaining the fundamental properties of the erythrocyte’s membrane cytoskeleton complex, the researchers wrote (Blood 2016;128:93-103).
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