(1) Iron overload can be regulated with tmprss6 siRNA because it induces hepcidin and diminishes iron in hemochromatosis. In this experiment, scientists used mice models with the HFE gene and treated them with tmprss6 siRNA formed in LNPs to increase hepcidin and lessen the iron intake. (2) Tmprss6 or matriptase-2, modulates negative hepcidin production. This mutation in both humans and mice, results in excess hepcidin expression and iron deficiency anemia. In doing so, tmprss6 is thought to regulate the pathway for iron-dependent of hepcidin. Targeted tmprss6 deletion in humans and mice not only decreases iron loading, but also reduces ineffective and erythropoiesis and splenomegaly, improving anemia.
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2. "An RNAi Therapeutic Targeting Tmprss6 Decreases Iron Overload in Hfe−/− Mice and Ameliorates Anemia and Iron Overload in Murine β-thalassemia Intermedia." An RNAi Therapeutic Targeting Tmprss6 Decreases Iron Overload in Hfe−/− Mice and Ameliorates Anemia and Iron Overload in Murine β-thalassemia Intermedia. N.p., n.d. Web. 27 May 2013. <http://bloodjournal.hematologylibrary.org/content/121/7/1200.full>.
2. "An RNAi Therapeutic Targeting Tmprss6 Decreases Iron Overload in Hfe−/− Mice and Ameliorates Anemia and Iron Overload in Murine β-thalassemia Intermedia." An RNAi Therapeutic Targeting Tmprss6 Decreases Iron Overload in Hfe−/− Mice and Ameliorates Anemia and Iron Overload in Murine β-thalassemia Intermedia. N.p., n.d. Web. 27 May 2013. <http://bloodjournal.hematologylibrary.org/content/121/7/1200.full>.