Heart Ferroportin Protein Content Is Regulated by Heart Iron Concentration and Systemic Hepcidin Expression.

The purpose of the study was to investigate the expression of ferroportin protein following treatments that affect systemic hepcidin. Administration of erythropoietin to C57BL/6J mice decreased systemic hepcidin expression; it also increased heart ferroportin protein content, determined by immunoblot in the membrane fraction, to approximately 200% of control values. This increase in heart ferroportin protein is very probably caused by a decrease in systemic hepcidin expression, in accordance with the classical regulation of ferroportin by hepcidin.

Oral health in a context of public health: prevention-related issue.

This publication analyses current literary knowledge on selected topics in the fields of oral health and pathology, with a particular emphasis on the potential roles of the oral microbiome and preventative approaches to oral afflictions. An important association with floral dysbiosis has been documented in important oral conditions, sometimes as a predisposing factor and at other times as a result thereof. However, much remains to be elucidated regarding the specific mechanisms at play, as well as their meaning in clinical practice.

Effect of Erythropoietin on the Expression of Murine Transferrin Receptor 2.

Erythropoietin (EPO) downregulates hepcidin expression to increase the availability of iron; the downregulation of hepcidin is mediated by erythroferrone (ERFE) secreted by erythroblasts. Erythroblasts also express transferrin receptor 2 (TFR2); however, the possible role of TFR2 in hepcidin downregulation is unclear. The purpose of the study was to correlate liver expression of hepcidin with the expression of ERFE and TFR2 in murine bone marrow and spleen at 4, 16, 24, 48, 72 and 96 h following administration of a single dose of EPO.