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Scientists have long thought that hematopoietic stem cells (HSCs) are regulated similarly in males and females.
But research conducted in mice has shown that HSCs exhibit sex differences in cell-cycle regulation.
The researchers discovered that HSCs in female mice divided significantly more frequently than HSCs in male mice, and this appeared to be driven by estrogen.
Sean Morrison, PhD, of UT Southwestern Medical Center in Dallas, and his colleagues detailed these discoveries in a letter to Nature.
The research suggested that differences in HSC division depend on the ovaries and not the testes. When the investigators administered estradiol, a hormone produced mainly in the ovaries, to male and female mice, HSC division increased in both sexes.
And experiments in pregnant mice highlighted the importance of estrogen in HSC activity. Estrogen levels increased during pregnancy, which increased HSC division, HSC frequency, cellularity, and erythropoiesis in the spleen.
“Elevated estrogen levels that are sustained during pregnancy induce stem cell mobilization and red cell production in the spleen, which serves as a reserve site for additional red blood cell production,” Dr Morrison said.
He and his colleagues also found that HSCs expressed high levels of estrogen receptor-alpha. And deleting the receptor reduced HSC division in female mice but not in males.
In pregnant mice, deleting the receptor attenuated the previously observed increases in HSC division, HSC frequency, and erythropoiesis.
These results suggest estrogen acts directly on HSCs to increase their proliferation and the number of red blood cells they generate.
“If estrogen has the same effect on stem cells in humans as in mice, then this effect raises a number of possibilities that could change the way we treat people with diseases of blood cell formation,” Dr Morrison said.
“Can we promote regeneration in the blood-forming system by administering estrogen? Can we reduce the toxicity of chemotherapy to the blood-forming system by taking into account estrogen levels in female patients? Does estrogen promote the growth of some blood cancers? There are numerous clinical opportunities to pursue.” 
Scientists have long thought that hematopoietic stem cells (HSCs) are regulated similarly in males and females.
But research conducted in mice has shown that HSCs exhibit sex differences in cell-cycle regulation.
The researchers discovered that HSCs in female mice divided significantly more frequently than HSCs in male mice, and this appeared to be driven by estrogen.
Sean Morrison, PhD, of UT Southwestern Medical Center in Dallas, and his colleagues detailed these discoveries in a letter to Nature.
The research suggested that differences in HSC division depend on the ovaries and not the testes. When the investigators administered estradiol, a hormone produced mainly in the ovaries, to male and female mice, HSC division increased in both sexes.
And experiments in pregnant mice highlighted the importance of estrogen in HSC activity. Estrogen levels increased during pregnancy, which increased HSC division, HSC frequency, cellularity, and erythropoiesis in the spleen.
“Elevated estrogen levels that are sustained during pregnancy induce stem cell mobilization and red cell production in the spleen, which serves as a reserve site for additional red blood cell production,” Dr Morrison said.
He and his colleagues also found that HSCs expressed high levels of estrogen receptor-alpha. And deleting the receptor reduced HSC division in female mice but not in males.
In pregnant mice, deleting the receptor attenuated the previously observed increases in HSC division, HSC frequency, and erythropoiesis.
These results suggest estrogen acts directly on HSCs to increase their proliferation and the number of red blood cells they generate.
“If estrogen has the same effect on stem cells in humans as in mice, then this effect raises a number of possibilities that could change the way we treat people with diseases of blood cell formation,” Dr Morrison said.
“Can we promote regeneration in the blood-forming system by administering estrogen? Can we reduce the toxicity of chemotherapy to the blood-forming system by taking into account estrogen levels in female patients? Does estrogen promote the growth of some blood cancers? There are numerous clinical opportunities to pursue.”
Scientists have long thought that hematopoietic stem cells (HSCs) are regulated similarly in males and females.
But research conducted in mice has shown that HSCs exhibit sex differences in cell-cycle regulation.
The researchers discovered that HSCs in female mice divided significantly more frequently than HSCs in male mice, and this appeared to be driven by estrogen.
Sean Morrison, PhD, of UT Southwestern Medical Center in Dallas, and his colleagues detailed these discoveries in a letter to Nature.
The research suggested that differences in HSC division depend on the ovaries and not the testes. When the investigators administered estradiol, a hormone produced mainly in the ovaries, to male and female mice, HSC division increased in both sexes.
And experiments in pregnant mice highlighted the importance of estrogen in HSC activity. Estrogen levels increased during pregnancy, which increased HSC division, HSC frequency, cellularity, and erythropoiesis in the spleen.
“Elevated estrogen levels that are sustained during pregnancy induce stem cell mobilization and red cell production in the spleen, which serves as a reserve site for additional red blood cell production,” Dr Morrison said.
He and his colleagues also found that HSCs expressed high levels of estrogen receptor-alpha. And deleting the receptor reduced HSC division in female mice but not in males.
In pregnant mice, deleting the receptor attenuated the previously observed increases in HSC division, HSC frequency, and erythropoiesis.
These results suggest estrogen acts directly on HSCs to increase their proliferation and the number of red blood cells they generate.
“If estrogen has the same effect on stem cells in humans as in mice, then this effect raises a number of possibilities that could change the way we treat people with diseases of blood cell formation,” Dr Morrison said.
“Can we promote regeneration in the blood-forming system by administering estrogen? Can we reduce the toxicity of chemotherapy to the blood-forming system by taking into account estrogen levels in female patients? Does estrogen promote the growth of some blood cancers? There are numerous clinical opportunities to pursue.”