Interracial contact shapes racial bias in the learning of person-knowledge.

During impression formation, perceptual cues facilitate social categorization while person-knowledge can promote individuation and enhance person memory. Although there is extensive literature on the cross-race recognition deficit, observed when racial ingroup faces are recognized more than outgroup faces, it is unclear whether a similar deficit exists when recalling individuating information about outgroup members. To better understand how perceived race can bias person memory, the present study examined how self-identified White perceivers' interracial contact impacts learning of perceptual cues and person-knowledge about perceived Black and White others over five sessions of training.

Calcium and IL-6 regulate the anterograde trafficking and plasma membrane residence of the iron exporter ferroportin to modulate iron efflux.

Iron is an essential element for proper cell functioning, but unbalanced levels can cause cell death. Iron metabolism is controlled at the blood-tissue barriers provided by microvascular endothelial cells. Dysregulated iron metabolism at these barriers is a factor in both neurodegenerative and cardiovascular diseases.

Transferrin Receptor Is Necessary for Proper Oligodendrocyte Iron Homeostasis and Development.

To test the hypothesis that the transferrin (Tf) cycle has unique importance for oligodendrocyte development and function, we disrupted the expression of the Tf receptor (Tfr) gene in oligodendrocyte progenitor cells (OPCs) on mice of either sex using the system. This ablation results in the elimination of iron incorporation via the Tf cycle but leaves other Tf functions intact. Mice lacking Tfr, specifically in NG2 or Sox10-positive OPCs, developed a hypomyelination phenotype.

Inflammation, dysregulated iron metabolism, and cardiovascular disease.

Iron is an essential trace element associated with both pathologic deficiency and toxic overload. Thus, systemic and cell iron metabolism are highly controlled processes regulated by protein expression and localization, as well as turnover, through the action of cytokines and iron status. Iron metabolism in the heart is challenging because both iron overload and deficiency are associated with cardiac disease.

Calcium and the Ca-ATPase SPCA1 modulate plasma membrane abundance of ZIP8 and ZIP14 to regulate Mn(II) uptake in brain microvascular endothelial cells.

Manganese (II) accumulation in human brain microvascular endothelial cells is mediated by the metal-ion transporters ZRT IRT-like protein 8 (ZIP8) and ZRT IRT-like protein 14 (ZIP14). The plasma membrane occupancy of ZIP14, in particular, is increased in cells treated with Mn, lipopolysaccharide, or IL-6, but the mechanism of this regulation has not been elucidated. The calcium-transporting type 2C member 1 ATPase, SPCA1, is a Golgi-localized Ca-uptake transporter thought to support Golgi uptake of Mn also.

Aberrant Cerebral Iron Trafficking Co-morbid With Chronic Inflammation: Molecular Mechanisms and Pharmacologic Intervention.

The redox properties that make iron an essential nutrient also make iron an efficient pro-oxidant. Given this nascent cytotoxicity, iron homeostasis relies on a combination of iron transporters, chaperones, and redox buffers to manage the non-physiologic aqueous chemistry of this first-row transition metal. Although a mechanistic understanding of the link between brain iron accumulation (BIA) and neurodegenerative diseases is lacking, BIA is co-morbid with the majority of cognitive and motor function disorders.

H-ferritin expression in astrocytes is necessary for proper oligodendrocyte development and myelination.

How iron is delivered to the CNS for myelination is poorly understood. Astrocytes are the most abundant glial cells in the brain and are the only cells in close contact with blood vessels. Therefore, they are strategically located to obtain nutrients, such as iron, from circulating blood.

Impaired Postnatal Myelination in a Conditional Knockout Mouse for the Ferritin Heavy Chain in Oligodendroglial Cells.

To define the importance of iron storage in oligodendrocyte development and function, the ferritin heavy subunit (Fth) was specifically deleted in oligodendroglial cells. Blocking Fth synthesis in Sox10 or NG2-positive oligodendrocytes during the first or the third postnatal week significantly reduces oligodendrocyte iron storage and maturation. The brain of Fth KO animals presented an important decrease in the expression of myelin proteins and a substantial reduction in the percentage of myelinated axons.