Cells like to move it, move it
Cell migration is important to diverse processes such as embryonic development, wound healing and cancer metastasis. The protein cortactin regulates cell migration – and promotes tumor cell invasion – but the underlying mechanisms for its actions are not clear.
Alissa Weaver, M.D., Ph.D., and colleagues explored the idea that cortactin regulates cell motility through a role in membrane trafficking – the movement of proteins and other components to the cell surface. They report in the Sept. 13 Current Biology that cortactin-deficient cells exhibit decreased secretion of fibronectin, part of the extracellular matrix (ECM, the “glue” through which cells migrate). They found that fibronectin accumulated within the cell, in a late endocytic/lysosomal compartment. The decreased secretion of fibronectin leads to defects in cell motility and in the lamellipodia (the moving edge of the cell).
The findings suggest that cortactin regulates cell motility by promoting ECM secretion, providing a link between cortactin’s reported functions in cell motility and membrane trafficking.
— Leigh MacMillan
Host countermeasure hinders HIVThe human body has innate mechanisms to combat viral infection. One such defense mechanism, the enzyme APOBEC3G (A3G), fights off HIV. But HIV fights back with a countermeasure called virion infectivity factor (Vif) to try to deplete A3G from cells. The one known mechanism by which A3G blocks HIV does not impair virus production from infected cells. Instead, it makes the viral particles (virions) produced by an infected cell unable to infect the next target human cell.
Richard D’Aquila, M.D., Kenneth Martin, Ph.D., and colleagues now find that A3G has an additional mechanism to stop HIV. They found that large aggregates of A3G and other cellular components (called A3G complexes) can decrease the number of virions produced from an infected cell.
The results, reported in the Sept. 1 Journal of Virology, suggest additional ways to boost anti-HIV effects of members of the APOBEC3 family for innovative therapeutic or preventive strategies against HIV.
— Melissa Marino
Getting the right fit for hearing aids
Hearing aids are commonly used to address communication difficulties in people with hearing loss. One goal in fitting hearing aids is to restore audibility to portions of speech that, because of the hearing loss, would otherwise be inaudible.
Benjamin Hornsby, Ph.D., and colleagues examined how degree of hearing loss and its configuration (the pattern of loss across sound frequencies) impacted benefit from amplified speech. They tested 62 adults with a wide range of high- and low-frequency hearing losses.
In the September/October issue of Ear & Hearing, they report that the configuration of hearing loss affects our ability to use speech information in different frequency regions. They found that extending high-frequency amplification improved, or did not degrade, speech understanding in all cases except for individuals with very steeply sloping losses (good low- but very poor high-frequency hearing). Individuals with flat hearing losses (similar loss at all frequencies) benefited most from extending high-frequency amplification. These findings have implications for hearing aid prescriptive fitting formulas.
— Leigh MacMillan
Cells at heart of infant lung disease
Around 60 percent of preterm infants born before 28 weeks are affected by bronchopulmonary dysplasia (BPD), a chronic lung disorder resulting from arrested lung development. While inflammatory processes appear to be involved, the cells responsible for initiating the immune response are unclear.
Lawrence Prince, M.D., Ph.D., and colleagues are using tissue cultures and mouse models to investigate the mediators of this disease process. In the Sept. 1 issue of The Journal of Immunology, they report that macrophages (immune cells that reside in the tissues instead of circulating in the blood) in fetal lung are the primary cellular site of this immune response. Activation of these macrophages inhibits development of fetal mouse airways, and macrophage depletion or inactivation of the NF-kappaB signaling pathway protects the developing airways in cultured lung tissue.
The findings demonstrate that activation of fetal lung macrophages initiates the inflammatory responses that disrupt signals critical for lung development – and suggest signaling pathways that might be targeted therapeutically to prevent or reverse the disease process.
— Melissa Marino
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