| First Author | Krieg L | Year | 2011 |
| Journal | Blood | Volume | 118 |
| Issue | 24 | Pages | 6418-25 |
| PubMed ID | 21976678 | Mgi Jnum | J:179090 |
| Mgi Id | MGI:5301055 | Doi | 10.1182/blood-2011-04-350082 |
| Citation | Krieg L, et al. (2011) Mutation of the gastric hydrogen-potassium ATPase alpha subunit causes iron-deficiency anemia in mice. Blood 118(24):6418-25 |
| abstractText | Iron is an essential component of heme and hemoglobin, and therefore restriction of iron availability directly limits erythropoiesis. In the present study, we report a defect in iron absorption that results in iron-deficiency anemia, as revealed by an N-ethyl-N-nitrosourea-induced mouse phenotype called sublytic. Homozygous sublytic mice develop hypochromic microcytic anemia with reduced osmotic fragility of RBCs. The sublytic phenotype stems from impaired gastrointestinal iron absorption caused by a point mutation of the gastric hydrogen-potassium ATPase alpha subunit encoded by Atp4a, which results in achlorhydria. The anemia of sublytic homozygotes can be corrected by feeding with a high-iron diet or by parenteral injection of iron dextran; rescue can also be achieved by providing acidified drinking water to sublytic homozygotes. These findings establish the necessity of the gastric proton pump for iron absorption and effective erythropoiesis. |
