Research article

Selenoproteins regulate macrophage invasiveness and extracellular matrix-related gene expression

Bradley A Carlson¹ , Min-Hyuk Yoo¹ , Yasuyo Sano² , Aniruddha Sengupta¹ , Jin Young Kim¹ , Robert Irons¹ , Vadim N Gladyshev³ , Dolph L Hatfield¹ and Jin Mo Park²

¹Molecular Biology of Selenium Section, Laboratory of Cancer Prevention, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA

²Cutaneous Biology Research Center, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA 02129, USA

³Department of Biochemistry, University of Nebraska, Lincoln, NE 68588, USA

author email corresponding author email

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

Published:	28 October 2009

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.