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The Journal of Neuroscience, June 6, 2007, 27(23):6207-6211; doi:10.1523/JNEUROSCI.1153-07.2007

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Brief Communications
Deletion of Apolipoprotein E Receptor-2 in Mice Lowers Brain Selenium and Causes Severe Neurological Dysfunction and Death When a Low-Selenium Diet Is Fed

Raymond F. Burk,¹ Kristina E. Hill,¹ Gary E. Olson,² Edwin J. Weeber,³ Amy K. Motley,¹ Virginia P. Winfrey,² and Lori M. Austin¹

¹Division of Gastroenterology, Hepatology, and Nutrition, Department of Medicine, ²Department of Cell and Developmental Biology, and ³Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, Tennessee 37232

Correspondence should be addressed to Raymond F. Burk, 1030C Medical Research Building IV, Vanderbilt Medical Center, Nashville, TN 37232-0252. Email: raymond.burk{at}vanderbilt.edu

Selenoprotein P (Sepp1) is a plasma and extracellular protein that is rich in selenium. Deletion of Sepp1 results in sharp decreases of selenium levels in the brain and testis with dysfunction of those organs. Deletion of Sepp1 also causes increased urinary selenium excretion, leading to moderate depletion of whole-body selenium. The lipoprotein receptor apolipoprotein E receptor-2 (apoER2) binds Sepp1 and facilitates its uptake by Sertoli cells, thus providing selenium for spermatogenesis. Experiments were performed to assess the effect of apoER2 on the concentration and function of selenium in the brain and on whole-body selenium. ApoER2^–/– and apoER2^+/+ male mice were fed a semipurified diet with selenite added as the source of selenium. ApoER2^–/– mice had depressed brain and testis selenium, but normal levels in liver, kidney, muscle, and the whole body. Feeding a selenium-deficient diet to apoER2^–/– mice led to neurological dysfunction and death, with some of the characteristics exhibited by Sepp1^–/– mice fed the same diet. Thus, although it does not affect whole-body selenium, apoER2 is necessary for maintenance of brain selenium and for prevention of neurological dysfunction and death under conditions of selenium deficiency, suggesting an interaction of apoER2 with Sepp1 in the brain.

Key words: brain selenium deficiency; neurological dysfunction; apoER2 knock-out; selenoprotein P; low selenium intake; normal whole-body selenium

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Received March 14, 2007; revised April 30, 2007; accepted May 5, 2007.

Correspondence should be addressed to Raymond F. Burk, 1030C Medical Research Building IV, Vanderbilt Medical Center, Nashville, TN 37232-0252. Email: raymond.burk{at}vanderbilt.edu

This article has been cited by other articles:

				G. E. Olson, V. P. Winfrey, K. E. Hill, and R. F. Burk Megalin Mediates Selenoprotein P Uptake by Kidney Proximal Tubule Epithelial Cells J. Biol. Chem., March 14, 2008; 283(11): 6854 - 6860. [Abstract] [Full Text] [PDF]

				Y. Zhang, Y. Zhou, U. Schweizer, N. E. Savaskan, D. Hua, J. Kipnis, D. L. Hatfield, and V. N. Gladyshev Comparative Analysis of Selenocysteine Machinery and Selenoproteome Gene Expression in Mouse Brain Identifies Neurons as Key Functional Sites of Selenium in Mammals J. Biol. Chem., January 25, 2008; 283(4): 2427 - 2438. [Abstract] [Full Text] [PDF]

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