Selenoproteins regulate macrophage invasiveness and extracellular matrix-related gene expression

Authors

Bradley A. Carlson, National Institutes of Health, Bethesda, MarylandFollow
Min-Hyuk Yoo, National Institutes of Health, Bethesda, MarylandFollow
Yasuyo Sano, Harvard UniversityFollow
Aniruddha Sengupta, National Institutes of Health, Bethesda, MarylandFollow
Jin Young Kim, National Institutes of Health, Bethesda, MarylandFollow
Robert Irons, National Institutes of Health, Bethesda, MarylandFollow
Vadim N. Gladyshev, University of Nebraska-LincolnFollow
Dolph L. Hatfield, National Institutes of Health, Bethesda, MarylandFollow
Jin Mo Park, Harvard UniversityFollow

Date of this Version

10-2009

Comments

Published in BMC Immunology 2009, 10:57 doi:10.1186/1471-2172-10-57

Abstract

Background: Selenium, a micronutrient whose deficiency in diet causes immune dysfunction and inflammatory disorders, is thought to exert its physiological effects mostly in the form of selenium-containing proteins (selenoproteins). Incorporation of selenium into the amino acid selenocysteine (Sec), and subsequently into selenoproteins is mediated by Sec tRNA^[Ser]Sec.
Results: To define macrophage-specific selenoprotein functions, we generated mice with the Sec tRNA^[Ser]Sec gene specifically deleted in myeloid cells. These mutant mice were devoid of the "selenoproteome" in macrophages, yet exhibited largely normal inflammatory responses. However, selenoprotein deficiency led to aberrant expression of extracellular matrix-related genes, and diminished migration of macrophages in a protein gel matrix.
Conclusion: Selenium status may affect immune defense and tissue homeostasis through its effect on selenoprotein expression and the trafficking of tissue macrophages.