This divide between the sexes is attributed to sex hormones, namely estrogen and testosterone. Both hormones are present in men and women, but testosterone predominates in males while estrogen predominates in females. Several organs in the body contain cells whose behavior is modulated by biological sex. For example, female muscle stem cells were found to regenerate muscle cells more efficiently than their male counterparts in a mouse model of muscular dystrophy. Though sex can influence cellular behavior in multiple organs, cells within organs that are not known to present sex-specific differences are thought to function similarly in both men and women.
However, a recent report in Nature challenges this notion. Studies in the Morrison lab at the University of Michigan have focused on identifying sex-specific differences in cell populations that are seemingly unresponsive to sex hormones, and hematopoietic stem cells, or HSCs, first grabbed the lab’s attention. Hematopoietic stem cells reside in the bone marrow and divide to generate red blood cells, which carry oxygen to tissues throughout the body, and immune cells, which recognize and destroy bacteria, viruses, and parasites. These cells often lie dormant until stimulated to divide by external cues, and there has been no previous evidence that these cells exhibit sex-related differences. Surprisingly, data from the Morrison group suggest that HSC behavior is not uniform between males and females. Though HSC number and frequency in male and female mice were comparable, increased HSC division was observed in female mice. Interestingly, HSC division was induced by administration of estrogen to both male and female mice, and this phenomenon did not occur in other bone marrow cell populations or in response to testosterone. HSC number, along with red blood cell and immune cell numbers, were increased in pregnant females compared to non-pregnant females. This effect was abolished when estrogen receptor function was compromised, leading to the theory that female HSCs respond to estrogen and that estrogen can regulate HSC division to accommodate the increased need for oxygen in pregnant females.
If these data mirror HSC activity in humans, there are several implications. First, the ability of HSCs to respond to estrogen may be relevant for the health of pregnant mothers and their unborn children. Estrogen levels among women can vary, so those with lower estrogen levels may be predisposed to more physical stresses during pregnancy. Second, there is now the possibility that sex hormones can modulate the onset of blood disorders and other diseases. For example, cytopenias, diseases in which immune cell numbers are greatly reduced, tend to be more common in men. Thus, reduced HSC proliferation in men might contribute to the persistence of these disorders. Third, sex may be an additional variable to consider in the field of personalized medicine, which involves the administration of therapy tailored to an individual’s genetic makeup. In this case, it will be imperative to note the individual’s sex in order to uncover contributing factors to disease and to predict patient prognosis.
Evolution allows organisms to meet metabolic needs during fluctuations in nutrient availability or changes in physical state (such as pregnancy). It is remarkable that nature may have designed a system that enables HSCs to divide in response to a sex hormone heavily involved in the reproductive process, and new insights provided by future studies on this topic will be of great interest. It will also be fascinating to discover other stem cell populations that function in a similar fashion. Until then, it is comforting to think that womanhood just got a lot better!
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