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Difference between revisions of "Fischer 2022 MitoFit Fe"

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{{MitoFit page name}}
{{Publication
{{Publication
|title=Fischer C, Valente de Souza L, Komlódi T, Garcia-Souza LF, Volani C, Tymoszuk P, Demetz E, Seifert M, Auer K, Hilbe R, Brigo N, Petzer V, Asshoff M, Gnaiger E, Weiss G (2022) Mitochondrial respiration in response to iron deficiency anemia. Comparison of peripheral blood mononuclear cells and liver. MitoFit Fe PBMCs liver 2022.2.
|title=Fischer C, Valente de Souza L, Komlódi T, Garcia-Souza LF, Volani C, Tymoszuk P, Demetz E, Seifert M, Auer K, Hilbe R, Brigo N, Petzer V, Asshoff M, Gnaiger E, Weiss G (2022) Mitochondrial respiration in response to iron deficiency anemia. Comparison of peripheral blood mononuclear cells and liver. MitoFit Preprints 2022.2. [[doi:10.26124/mitofit:2022-0002]]
|authors=Fischer Christine, Valente de Souza Lara, Komlódi T, Garcia-Souza Luiz F, Volani Chiara, Tymoszuk Piotr, Demetz Egon, Seifert Markus, Auer Kristina, Hilbe Richard, Brigo Natascha, Petzer Verena, Asshoff Malte, Gnaiger Erich, Weiss Guenter
|info=[[File:MitoFit Preprints pdf.png|left|160px|link=  |MitoFit pdf]] [Mitochondrial respiration in response to iron deficiency anemia. Comparison of peripheral blood mononuclear cells and liver]<br/>
|authors=Fischer Christine, Valente de Souza Lara, Komlódi Timea, Garcia-Souza Luiz F, Volani Chiara, Tymoszuk Piotr, Demetz Egon, Seifert Markus, Auer Kristina, Hilbe Richard, Brigo Natascha, Petzer Verena, Asshoff Malte, Gnaiger Erich, Weiss Guenter
|year=2022-03-03
|year=2022-03-03
|journal=MitoFit Prep
|journal=MitoFit Prep
|abstract=Iron is an essential component for metabolic processes including oxygen transport within hemoglobin, tricarboxylic acid (TCA) cycle activity and mitochondrial energy transformation. Iron deficiency can thus lead to metabolic dysfunction and eventually result in iron deficiency anemia (IDA) which affects approximately 1.5 billion people worldwide. Using a rat model of IDA induced by phlebotomy, we studied the effects of IDA on mito-chondrial respiration in peripheral blood mononuclear cells (PBMCs) and liver. Furthermore, we evaluated whether mitochondrial function evaluated by high-resolution respirometry in PBMCs reflects corresponding alterations in the liver. Surprisingly, mitochondrial respiratory capacity was increased in PBMCs from rats with IDA compared to controls. In contrast, mitochondrial respiration remained unaffected in livers from IDA rats. Of note, citrate synthase activity indicated an increased mitochondrial density in PBMCs, whereas it remained unchanged in the liver, partly explaining the different responses of mitochondrial respiration in PBMCs and liver. Taken together, these results indicate that mitochondrial function determined in PBMCs cannot serve as a valid surrogate for respiration in the liver. Metabolic adaptions to iron deficiency resulted in different metabolic reprogramming in the blood cells and liver tissue.
|abstract=Iron is an essential component for metabolic processes including oxygen transport within hemoglobin, tricarboxylic acid (TCA) cycle activity and mitochondrial energy transformation. Iron deficiency can thus lead to metabolic dysfunction and eventually result in iron deficiency anemia (IDA) which affects approximately 1.5 billion people worldwide. Using a rat model of IDA induced by phlebotomy, we studied the effects of IDA on mito-chondrial respiration in peripheral blood mononuclear cells (PBMCs) and liver. Furthermore, we evaluated whether mitochondrial function evaluated by high-resolution respirometry in PBMCs reflects corresponding alterations in the liver. Surprisingly, mitochondrial respiratory capacity was increased in PBMCs from rats with IDA compared to controls. In contrast, mitochondrial respiration remained unaffected in livers from IDA rats. Of note, citrate synthase activity indicated an increased mitochondrial density in PBMCs, whereas it remained unchanged in the liver, partly explaining the different responses of mitochondrial respiration in PBMCs and liver. Taken together, these results indicate that mitochondrial function determined in PBMCs cannot serve as a valid surrogate for respiration in the liver. Metabolic adaptions to iron deficiency resulted in different metabolic reprogramming in the blood cells and liver tissue.
<br><br>
|keywords=anemia, iron deficiency, peripheral blood mononuclear cells, liver, mitochondrial function, OXPHOS, mitochondrial respiration, surrogate
|keywords=anemia, iron deficiency, peripheral blood mononuclear cells, liver, mitochondrial function, OXPHOS, mitochondrial respiration, surrogate
|editor=Doerrier C
|editor=Doerrier C
|mipnetlab=AT Innsbruck Oroboros
|mipnetlab=AT Innsbruck Oroboros
}}
}}
ORC'''ID''': [[File:ORCID.png|20px|link=https://orcid.org/0000-0002-5656-5030]] Fischer Christine, [[File:ORCID.png|20px|link=https://orcid.org/0000-0001-9876-1411]] Komlódi Timea, [[File:ORCID.png|20px|link=https://orcid.org/0000-0003-1474-5428]] Garcia-Souza Luiz F, [[File:ORCID.png|20px|link=https://orcid.org/0000-0003-3600-4735]] Volani Chiara, [[File:ORCID.png|20px|link=https://orcid.org/0000-0002-0398-6034]] Tymoszuk Piotr, [[File:ORCID.png|20px|link=https://orcid.org/0000-0002-5723-927X]] Demetz Egon, [[File:ORCID.png|20px|link=https://orcid.org/0000-0003-3647-5895]] Gnaiger Erich, [[File:ORCID.png|20px|link=https://orcid.org/0000-0003-0709-2158]] Weiss Guenter
__TOC__
== Data availability ==
:::: Original files are not provided by the authors.
== Support ==
:::: This research was funded by the Christian Doppler Laboratory for Iron Metabolism and Anemia Research, the FWF funded doctoral program HOROS (W-1253, to GW) and the transnational doctoral program BI-DOC between the Medical University of Innsbruck, Austria and the Institute of Biomedicine, Eurac, in Bolzano, Italy.
{{Labeling
{{Labeling
|area=Respiration
|area=Respiration

Revision as of 13:57, 3 March 2022


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Fischer 2022 MitoFit Fe


Publications in the MiPMap
Fischer C, Valente de Souza L, Komlódi T, Garcia-Souza LF, Volani C, Tymoszuk P, Demetz E, Seifert M, Auer K, Hilbe R, Brigo N, Petzer V, Asshoff M, Gnaiger E, Weiss G (2022) Mitochondrial respiration in response to iron deficiency anemia. Comparison of peripheral blood mononuclear cells and liver. MitoFit Preprints 2022.2. doi:10.26124/mitofit:2022-0002

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[Mitochondrial respiration in response to iron deficiency anemia. Comparison of peripheral blood mononuclear cells and liver]

Fischer Christine, Valente de Souza Lara, Komlódi Timea, Garcia-Souza Luiz F, Volani Chiara, Tymoszuk Piotr, Demetz Egon, Seifert Markus, Auer Kristina, Hilbe Richard, Brigo Natascha, Petzer Verena, Asshoff Malte, Gnaiger Erich, Weiss Guenter (2022-03-03) MitoFit Prep

Abstract: Iron is an essential component for metabolic processes including oxygen transport within hemoglobin, tricarboxylic acid (TCA) cycle activity and mitochondrial energy transformation. Iron deficiency can thus lead to metabolic dysfunction and eventually result in iron deficiency anemia (IDA) which affects approximately 1.5 billion people worldwide. Using a rat model of IDA induced by phlebotomy, we studied the effects of IDA on mito-chondrial respiration in peripheral blood mononuclear cells (PBMCs) and liver. Furthermore, we evaluated whether mitochondrial function evaluated by high-resolution respirometry in PBMCs reflects corresponding alterations in the liver. Surprisingly, mitochondrial respiratory capacity was increased in PBMCs from rats with IDA compared to controls. In contrast, mitochondrial respiration remained unaffected in livers from IDA rats. Of note, citrate synthase activity indicated an increased mitochondrial density in PBMCs, whereas it remained unchanged in the liver, partly explaining the different responses of mitochondrial respiration in PBMCs and liver. Taken together, these results indicate that mitochondrial function determined in PBMCs cannot serve as a valid surrogate for respiration in the liver. Metabolic adaptions to iron deficiency resulted in different metabolic reprogramming in the blood cells and liver tissue.

Keywords: anemia, iron deficiency, peripheral blood mononuclear cells, liver, mitochondrial function, OXPHOS, mitochondrial respiration, surrogate Bioblast editor: Doerrier C O2k-Network Lab: AT Innsbruck Oroboros

ORCID: ORCID.png Fischer Christine, ORCID.png Komlódi Timea, ORCID.png Garcia-Souza Luiz F, ORCID.png Volani Chiara, ORCID.png Tymoszuk Piotr, ORCID.png Demetz Egon, ORCID.png Gnaiger Erich, ORCID.png Weiss Guenter

Data availability

Original files are not provided by the authors.

Support

This research was funded by the Christian Doppler Laboratory for Iron Metabolism and Anemia Research, the FWF funded doctoral program HOROS (W-1253, to GW) and the transnational doctoral program BI-DOC between the Medical University of Innsbruck, Austria and the Institute of Biomedicine, Eurac, in Bolzano, Italy.


Labels: MiParea: Respiration  Pathology: Other 

Organism: Rat  Tissue;cell: Liver, Blood cells  Preparation: Permeabilized cells, Homogenate  Enzyme: Marker enzyme 

Coupling state: LEAK, ROUTINE, OXPHOS, ET  Pathway: N, S, NS, Other combinations, ROX  HRR: Oxygraph-2k