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Conrad, M. ; Bornkamm, G.W. ; Brielmeier, M.

Mitochondrial and cytosolic thioredoxin reductase knockout mice.

In: Selenium: Its Molecular Biology and Role in Human Health. New York: Springer, 2006. 195-206

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To address the role of the thioredoxin system in redox regulation of apoptosis and proliferation, mice with targeted deletions of both the cytosolic (Txnrd1) and the mitochondrial (Txnrd2) thioredoxin reductases were generated. These two selenoproteins are key enzymes governing the activities of cytosolic and mitochondrial thioredoxins, respectively, which are, in turn, implicated in a variety of cellular functions, such as cell-cell communication, proliferation and apoptosis. Ubiquitous and heart-specific inactivation revealed widely non-redundant functions of Txnrd1 and Txnrd2. A significant drop in cell proliferation rates throughout the embryo (except in the heart), but not increased apoptosis, was the underlying cause of embryonic death of Txnrd1 knockout embryos at E10.5. Perturbed cardiac development and increased apoptosis of fetal blood cells in the liver caused severe anemia, growth retardation and embryonic death (E13.5) in Txnrd2 knockout embryos. Cardiac-tissue restricted inactivation of Txnrd2 led to biventricular dilated cardiomyopathy and postnatal death; in contrast heart-specific inactivation of Txnrd1 had no apparent effect on the viability of the knockout mice. In conclusion, Txnrd1 contributes to cell proliferation, whereas Txnrd2 is rather involved in apoptosis regulation.