We welcome suggestions for research to highlight in Aliquots. The items should be primary research articles (no reviews, editorials or commentaries) published within the last two months in a peer-reviewed journal. Please send the article citation (PDF if available) and any other feedback about the column to: aliquots@vanderbilt.edu.
Water for strong bones?
Bone fractures are increasingly common as we age. Although this is often attributed to loss of bone mineral density (BMD), measurements of BMD cannot alone predict whether an individual is at risk of fracture, highlighting the need for improved measures of bone quality.
Jeffry Nyman, Ph.D., and colleagues have developed a nuclear magnetic resonance (NMR) technique to measure the amount of bound water and mobile water (found in microscopic pores) in bone. The team compared these NMR-derived measures of bone water distribution to measures of mechanical properties in femur bone samples from middle-aged and elderly male cadavers.
While there were no age-related changes in mobile water, the amount of bound water significantly decreased with age. Bound water was also associated with bone strength and toughness, while mobile water was correlated with elasticity. The results, available online in the journal Bone, suggest that measuring bound and mobile water within bone could be useful for determining bone quality and predicting one's potential for fracture.
— Melissa Marino
Cell division stems from diet
The axiom “you are what you eat” underscores the importance of diet on health. The body's stem cells, which are crucial for maintaining tissue integrity and function, may be particularly sensitive to dietary factors.
Daniela Drummond-Barbosa, Ph.D., and colleagues are examining how diet influences stem cells in the fruit fly ovary. They previously found that, when flies consume a protein-rich diet, insulin-like peptides (DILPs) produced in their brains directly enhance cell division in ovarian stem cells.
In the journal Developmental Biology, the researchers now provide additional detail about this process. They show that DILPs specifically control the G2 phase of cell division — the growth phase between DNA replication and cell division — while another unidentified diet-related factor regulates another cell cycle “growth” phase (G1).
They also found that tumors derived from ovarian stem cells respond similarly to diet through both pathways, suggesting a mechanism that may underlie the link between diet, insulin signaling and cancer risk in humans.
— Melissa Marino
The silence of the motor protein
Mutations in the motor protein myosin-1a (Myo1a) have been linked to non-syndromic human deafness — hearing loss often associated with defective structures in the inner ear.
Matthew Tyska, Ph.D., and colleagues examined the impact of one particular deafness mutation, E385D, on Myo1a function. They report in the Biophysical Journal that purified E385D-Myo1a has enzymatic activity that is slower than the wild-type protein, and that mutant Myo1a cannot move actin in an in vitro assay. They also showed in cultured cells that the mutation disrupts the ability of Myo1a to localize to cellular protrusions called microvilli, which is believed to be critical for Myo1a function in inner ear cells.
The authors conclude that these defects represent the molecular basis for hearing loss in individuals with the E385D mutation. They speculate that Myo1a plays roles that are important for inner ear cell function, such as stabilizing membrane-cytoskeleton interactions and transporting membrane proteins and lipids.
— Leigh MacMillan
Cells proliferate in the islands
During the production of red blood cells, precursor cells cluster around a single macrophage — a type of white blood cell — to form “erythroblastic islands.” Melissa Rhodes, M.D., Mark Koury, M.D., and colleagues reconstituted these islands in vitro, using macrophages and erythroblasts (red blood cell precursors) from a mouse model. They report in the journal Blood that erythroblasts that were co-cultured with macrophages produced three times the number of cells compared to erythroblasts cultured alone. This enhanced proliferation required direct contact with the macrophages, resulted from a faster transit through the cell cycle, and was due to a different mechanism than the anti-cell death effect of erythropoetin — the main regulator of erythroid progenitor numbers.
The results suggest a mechanism for the development of anemias associated with abnormal macrophage function, such as anemias of chronic inflammation and myelodysplasia, and for the reduced responsiveness of those anemias to erythropoeitin therapy.
— Leigh MacMillan
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