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Exacerbation of Neonatal Hemolysis and Impaired Renal Iron Handling in Heme Oxygenase 1-Deficient Mice
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 p...
Autores principales: | , , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7589678/ https://www.ncbi.nlm.nih.gov/pubmed/33092142 http://dx.doi.org/10.3390/ijms21207754 |
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author | Bednarz, Aleksandra Lipiński, Paweł Starzyński, Rafał R. Tomczyk, Mateusz Kraszewska, Izabela Herman, Sylwia Kowalski, Kacper Gruca, Ewelina Jończy, Aneta Mazgaj, Rafał Szudzik, Mateusz Rajfur, Zenon Baster, Zbigniew Józkowicz, Alicja Lenartowicz, Małgorzata |
author_facet | Bednarz, Aleksandra Lipiński, Paweł Starzyński, Rafał R. Tomczyk, Mateusz Kraszewska, Izabela Herman, Sylwia Kowalski, Kacper Gruca, Ewelina Jończy, Aneta Mazgaj, Rafał Szudzik, Mateusz Rajfur, Zenon Baster, Zbigniew Józkowicz, Alicja Lenartowicz, Małgorzata |
author_sort | Bednarz, Aleksandra |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-7589678 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-75896782020-10-29 Exacerbation of Neonatal Hemolysis and Impaired Renal Iron Handling in Heme Oxygenase 1-Deficient Mice Bednarz, Aleksandra Lipiński, Paweł Starzyński, Rafał R. Tomczyk, Mateusz Kraszewska, Izabela Herman, Sylwia Kowalski, Kacper Gruca, Ewelina Jończy, Aneta Mazgaj, Rafał Szudzik, Mateusz Rajfur, Zenon Baster, Zbigniew Józkowicz, Alicja Lenartowicz, Małgorzata Int J Mol Sci Article 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. MDPI 2020-10-20 /pmc/articles/PMC7589678/ /pubmed/33092142 http://dx.doi.org/10.3390/ijms21207754 Text en © 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Bednarz, Aleksandra Lipiński, Paweł Starzyński, Rafał R. Tomczyk, Mateusz Kraszewska, Izabela Herman, Sylwia Kowalski, Kacper Gruca, Ewelina Jończy, Aneta Mazgaj, Rafał Szudzik, Mateusz Rajfur, Zenon Baster, Zbigniew Józkowicz, Alicja Lenartowicz, Małgorzata Exacerbation of Neonatal Hemolysis and Impaired Renal Iron Handling in Heme Oxygenase 1-Deficient Mice |
title | Exacerbation of Neonatal Hemolysis and Impaired Renal Iron Handling in Heme Oxygenase 1-Deficient Mice |
title_full | Exacerbation of Neonatal Hemolysis and Impaired Renal Iron Handling in Heme Oxygenase 1-Deficient Mice |
title_fullStr | Exacerbation of Neonatal Hemolysis and Impaired Renal Iron Handling in Heme Oxygenase 1-Deficient Mice |
title_full_unstemmed | Exacerbation of Neonatal Hemolysis and Impaired Renal Iron Handling in Heme Oxygenase 1-Deficient Mice |
title_short | Exacerbation of Neonatal Hemolysis and Impaired Renal Iron Handling in Heme Oxygenase 1-Deficient Mice |
title_sort | exacerbation of neonatal hemolysis and impaired renal iron handling in heme oxygenase 1-deficient mice |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7589678/ https://www.ncbi.nlm.nih.gov/pubmed/33092142 http://dx.doi.org/10.3390/ijms21207754 |
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