Similarly to Us, Old Age Isn’t Kind to Hematopoietic Stem Cells Either

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Always thought to be able to self-renew indefinitely, hematopietic stem cells have been considered as an important multipotent source of cells able to generate a variety of cell types within a specific tissue family. Just last week, a group of scientists led by a University of Wisconsin-Madison stem cell researcher Igor Slukvin reported on the discovery of two groups of transcriptional regulators capable of inducing distinct differentiation of hematopoietic stem cells into hemogenic endothelial cells, which subsequently develop into various types of blood cells. The Nature Communications study is the first time transcription factors have been used to product different kinds of cells from hematopoietic stem cells.

Now, however, a remarkable Nature study – titled “Replication stress is a potent driver of functional decline in ageing haematopoietic stem cells” – described hematopoietic stem cells as not quite forever self-renewing. Led by Emmanuelle Passegué at the University of California San Francisco Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research, the study blamed stress as a cause for the functional decline in old hematopoietic stem cells. The reason for that is thought to be increased replication stress that occurs as a function of cell cycle defects and chromosome gaps. This results in decreased expression in mini chromosome maintenance DNA helicase, which in turn caused DNA damage and death.

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With a weakened immune system and a reduced functionality of their hematopoietic stem cells, this is ultimately the reason why old people are not donor candidates for bone marrow transplantation.

The study ultimately postulates that a drug that retains DNA helicase components to be a significant potential target for improved stem cell therapies and avoidance of immune system failure.

 

 

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