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in the bone marrow
Researchers say they have identified a protein that plays a key role in regulating hematopoietic stem cell (HSC) engraftment.
Experiments revealed that protein tyrosine phosphatase-sigma (PTP-sigma) suppresses normal HSC engraftment capacity, but targeted inhibition of
PTP-sigma can substantially improve mouse and human HSC engraftment.
The researchers described these findings in The Journal of Clinical Investigation.
Mamle Quarmyne, a graduate student at the University of California, Los Angeles, and her colleagues first found that PTP-sigma is expressed on a high percentage of mouse and human HSCs.
When the team deleted PTP-sigma in mice, they observed a marked increase in HSCs’ ability to engraft.
When they selected human HSCs that did not express PTP-sigma and transplanted these cells into immune-deficient mice, the researchers observed a 15-fold increase in HSC engraftment.
The team also discovered that PTP-sigma regulates HSC function by suppressing a protein called RAC1, which is known to promote HSC engraftment.
“These findings have tremendous therapeutic potential, since we have identified a new receptor on HSCs, PTP-sigma, which can be specifically targeted as a means to potently increase the engraftment of transplanted HSCs in patients,” said John P. Chute, MD, of the University of California, Los Angeles.
“This approach can also potentially accelerate hematologic recovery in cancer patients receiving chemotherapy and/or radiation, which also suppress the blood and immune systems.”
Now, the researchers are testing small molecules for their ability to inhibit PTP-sigma on HSCs. If these studies are successful, the team aims to translate these findings into clinical trials in the near future. 
in the bone marrow
Researchers say they have identified a protein that plays a key role in regulating hematopoietic stem cell (HSC) engraftment.
Experiments revealed that protein tyrosine phosphatase-sigma (PTP-sigma) suppresses normal HSC engraftment capacity, but targeted inhibition of
PTP-sigma can substantially improve mouse and human HSC engraftment.
The researchers described these findings in The Journal of Clinical Investigation.
Mamle Quarmyne, a graduate student at the University of California, Los Angeles, and her colleagues first found that PTP-sigma is expressed on a high percentage of mouse and human HSCs.
When the team deleted PTP-sigma in mice, they observed a marked increase in HSCs’ ability to engraft.
When they selected human HSCs that did not express PTP-sigma and transplanted these cells into immune-deficient mice, the researchers observed a 15-fold increase in HSC engraftment.
The team also discovered that PTP-sigma regulates HSC function by suppressing a protein called RAC1, which is known to promote HSC engraftment.
“These findings have tremendous therapeutic potential, since we have identified a new receptor on HSCs, PTP-sigma, which can be specifically targeted as a means to potently increase the engraftment of transplanted HSCs in patients,” said John P. Chute, MD, of the University of California, Los Angeles.
“This approach can also potentially accelerate hematologic recovery in cancer patients receiving chemotherapy and/or radiation, which also suppress the blood and immune systems.”
Now, the researchers are testing small molecules for their ability to inhibit PTP-sigma on HSCs. If these studies are successful, the team aims to translate these findings into clinical trials in the near future.
in the bone marrow
Researchers say they have identified a protein that plays a key role in regulating hematopoietic stem cell (HSC) engraftment.
Experiments revealed that protein tyrosine phosphatase-sigma (PTP-sigma) suppresses normal HSC engraftment capacity, but targeted inhibition of
PTP-sigma can substantially improve mouse and human HSC engraftment.
The researchers described these findings in The Journal of Clinical Investigation.
Mamle Quarmyne, a graduate student at the University of California, Los Angeles, and her colleagues first found that PTP-sigma is expressed on a high percentage of mouse and human HSCs.
When the team deleted PTP-sigma in mice, they observed a marked increase in HSCs’ ability to engraft.
When they selected human HSCs that did not express PTP-sigma and transplanted these cells into immune-deficient mice, the researchers observed a 15-fold increase in HSC engraftment.
The team also discovered that PTP-sigma regulates HSC function by suppressing a protein called RAC1, which is known to promote HSC engraftment.
“These findings have tremendous therapeutic potential, since we have identified a new receptor on HSCs, PTP-sigma, which can be specifically targeted as a means to potently increase the engraftment of transplanted HSCs in patients,” said John P. Chute, MD, of the University of California, Los Angeles.
“This approach can also potentially accelerate hematologic recovery in cancer patients receiving chemotherapy and/or radiation, which also suppress the blood and immune systems.”
Now, the researchers are testing small molecules for their ability to inhibit PTP-sigma on HSCs. If these studies are successful, the team aims to translate these findings into clinical trials in the near future.