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Article

Exacerbation of Neonatal Hemolysis and Impaired Renal Iron Handling in Heme Oxygenase 1-Deficient Mice

1
Department of Genetics and Evolution, Institute of Zoology and Biomedical Research, Jagiellonian University, Gronostajowa 9, 30-387 Kraków, Poland
2
Department of Molecular Biology, Institute of Genetics and Animal Biotechnology, Polish Academy of Sciences, Jastrzębiec, 05-552 Magdalenka, Poland
3
Department of Medical Biotechnology, Faculty of Biochemistry, Biophysics and Biotechnology, Jagiellonian University, Gronostajowa 7, 30-387 Kraków, Poland
4
Department of Molecular and Interfacial Biophysics, Faculty of Physics, Astronomy and Applied Computer Science, Jagiellonian University, Łojasiewicza 11, 30-348 Kraków, Poland
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2020, 21(20), 7754; https://doi.org/10.3390/ijms21207754
Received: 22 September 2020 / Revised: 15 October 2020 / Accepted: 16 October 2020 / Published: 20 October 2020
In most mammals, neonatal intravascular hemolysis is a benign and moderate disorder that usually does not lead to anemia. During the neonatal period, kidneys play a key role in detoxification and recirculation of iron species released from red blood cells (RBC) and filtered out by glomeruli to the primary urine. Activity of heme oxygenase 1 (HO1), a heme-degrading enzyme localized in epithelial cells of proximal tubules, seems to be of critical importance for both processes. We show that, in HO1 knockout mouse newborns, hemolysis was prolonged despite a transient state and exacerbated, which led to temporal deterioration of RBC status. In neonates lacking HO1, functioning of renal molecular machinery responsible for iron reabsorption from the primary urine (megalin/cubilin complex) and its transfer to the blood (ferroportin) was either shifted in time or impaired, respectively. Those abnormalities resulted in iron loss from the body (excreted in urine) and in iron retention in the renal epithelium. We postulate that, as a consequence of these abnormalities, a tight systemic iron balance of HO1 knockout neonates may be temporarily affected. View Full-Text
Keywords: iron; heme; heme oxygenase 1; Hmox1 gene; neonatal hemolysis; renal iron handling iron; heme; heme oxygenase 1; Hmox1 gene; neonatal hemolysis; renal iron handling
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MDPI and ACS Style

Bednarz, A.; Lipiński, P.; Starzyński, R.R.; Tomczyk, M.; Kraszewska, I.; Herman, S.; Kowalski, K.; Gruca, E.; Jończy, A.; Mazgaj, R.; Szudzik, M.; Rajfur, Z.; Baster, Z.; Józkowicz, A.; Lenartowicz, M. Exacerbation of Neonatal Hemolysis and Impaired Renal Iron Handling in Heme Oxygenase 1-Deficient Mice. Int. J. Mol. Sci. 2020, 21, 7754. https://doi.org/10.3390/ijms21207754

AMA Style

Bednarz A, Lipiński P, Starzyński RR, Tomczyk M, Kraszewska I, Herman S, Kowalski K, Gruca E, Jończy A, Mazgaj R, Szudzik M, Rajfur Z, Baster Z, Józkowicz A, Lenartowicz M. Exacerbation of Neonatal Hemolysis and Impaired Renal Iron Handling in Heme Oxygenase 1-Deficient Mice. International Journal of Molecular Sciences. 2020; 21(20):7754. https://doi.org/10.3390/ijms21207754

Chicago/Turabian Style

Bednarz, Aleksandra, Paweł Lipiński, Rafał R. Starzyński, Mateusz Tomczyk, Izabela Kraszewska, Sylwia Herman, Kacper Kowalski, Ewelina Gruca, Aneta Jończy, Rafał Mazgaj, Mateusz Szudzik, Zenon Rajfur, Zbigniew Baster, Alicja Józkowicz, and Małgorzata Lenartowicz. 2020. "Exacerbation of Neonatal Hemolysis and Impaired Renal Iron Handling in Heme Oxygenase 1-Deficient Mice" International Journal of Molecular Sciences 21, no. 20: 7754. https://doi.org/10.3390/ijms21207754

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