Submitted to: DNA and Cell Biology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 8/17/2000
Publication Date: 11/20/2000
Citation: Vallet, J.L., Fahrenkrug, S.C. 2000. Structure of the gene for uteroferrin. DNA and Cell Biology. 19(11):689-696.
Interpretive Summary: The uterus of the pig produces many proteins that deliver nutrients to the developing piglet during pregnancy. The most well studied of these, a protein called uteroferrin, delivers iron which is then used by the developing piglet for making red blood cells and other iron containing tissues. The amount of iron delivered to the piglet during pregnancy is controlled by the activity of the gene for uteroferrin, which in turn is controlled by information encoded in the gene itself. Furthermore, uteroferrin is one of the most abundant proteins secreted by the pig uterus, making the gene a good candidate for use in transgenic work targeting the uterus. The gene for uteroferrin has been isolated and characterized previously but recent work in our lab indicated that the reported characterization might be in error in several key points. We isolated and recharacterized the gene for uteroferrin and found several important descrepancies with that reported previously. Most important among these is that the region of the uteroferrin gene most likely controlling uteroferrin production was dramatically different from that reported previously, calling into question several experiments that have been performed based on the previously reported gene. It was concluded that the previous report was in error. These results are key to the future understanding of iron transport to the developing piglet during pregnancy, and to future work using the uteroferrin gene in transgenic approaches targeting the uterus.
Technical Abstract: Numerous studies with equivocal results have been performed to determine the effect of exogenous iron and folate on reproductive performance in swine. However, the effect of exogenous iron and folate on secretion of their respective uterine transport proteins has never been reported. Twenty gilts were infused (n = 5 per treatment) with either (1) saline, (2) alpha-tocopherol, (3) alpha-tocopherol plus iron citrate or (4) alpha-tocopherol plus tetrahydrofolate on d 11 to 14 of pregnancy. On d 14, blood samples were obtained at 0, 2, 4, 6, 8, and 24 h after infusion and samples were measured for plasma iron and folate. Gilts were slaughtered on d 15 and the reproductive tracts were recovered. Each uterine horn was flushed with 20 mL saline and the average number of somites within conceptuses from each flush was determined. Conceptus tissues were separated from the uterine flushings by centrifugation and the uterine flushings were measured for total protein, total retinol binding protein, total acid phosphatase and total folate binding protein. Intravenous infusion of iron citrate and tetrahydrofolate increased (P < 0.05) plasma iron and folate, respectively, for 6 to 8 h but had no effect on uterine content of uteroferrin or secreted folate binding protein. These data suggest that uterine secretion of uteroferrin and secreted folate binding protein are not influenced by plasma levels of iron and folate, respectively, and may provide an explanation for the equivocal effect of iron and folate treatment on reproductive performance in gilts.