Redox Metabolism and Vascular Calcification in Chronic Kidney Disease
Vascular calcification (VC) is a common complication in patients with chronic kidney disease which increases their mortality. Although oxidative stress is involved in the onset and progression of this disorder, the specific role of some of the main redox regulators, such as catalase, the main scaven...
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| Format: | Article |
| Language: | English |
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MDPI AG
2023-09-01
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| Series: | Biomolecules |
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| Online Access: | https://www.mdpi.com/2218-273X/13/9/1419 |
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| author | Natalia Carrillo-López Sara Panizo Beatriz Martín-Carro Juan Carlos Mayo Barrallo Pablo Román-García Raúl García-Castro Jesús María Fernández-Gómez Miguel Ángel Hevia-Suárez Julia Martín-Vírgala Sara Fernández-Villabrille Laura Martínez-Arias Sara Barrio Vázquez Laura Calleros Basilio Manuel Naves-Díaz Jorge Benito Cannata-Andía Isabel Quirós-González Cristina Alonso-Montes José Luis Fernández-Martín |
| author_facet | Natalia Carrillo-López Sara Panizo Beatriz Martín-Carro Juan Carlos Mayo Barrallo Pablo Román-García Raúl García-Castro Jesús María Fernández-Gómez Miguel Ángel Hevia-Suárez Julia Martín-Vírgala Sara Fernández-Villabrille Laura Martínez-Arias Sara Barrio Vázquez Laura Calleros Basilio Manuel Naves-Díaz Jorge Benito Cannata-Andía Isabel Quirós-González Cristina Alonso-Montes José Luis Fernández-Martín |
| author_sort | Natalia Carrillo-López |
| collection | DOAJ |
| description | Vascular calcification (VC) is a common complication in patients with chronic kidney disease which increases their mortality. Although oxidative stress is involved in the onset and progression of this disorder, the specific role of some of the main redox regulators, such as catalase, the main scavenger of H<sub>2</sub>O<sub>2</sub>, remains unclear. In the present study, epigastric arteries of kidney transplant recipients, a rat model of VC, and an in vitro model of VC exhibiting catalase (Cts) overexpression were analysed. Pericalcified areas of human epigastric arteries had increased levels of catalase and cytoplasmic, rather than nuclear runt-related transcription factor 2 (RUNX2). In the rat model, advanced aortic VC concurred with lower levels of the H<sub>2</sub>O<sub>2</sub>-scavenger glutathione peroxidase 3 compared to controls. In an early model of calcification using vascular smooth muscle cells (VSMCs), Cts VSMCs showed the expected increase in total levels of RUNX2. However, Cts VMSCs also exhibited a lower percentage of the nucleus stained for RUNX2 in response to calcifying media. In this early model of VC, we did not observe a dysregulation of the mitochondrial redox state; instead, an increase in the general redox state was observed in the cytoplasm. These results highlight the complex role of antioxidant enzymes as catalase by regulation of RUNX2 subcellular location delaying the onset of VC. |
| first_indexed | 2024-03-10T22:59:11Z |
| format | Article |
| id | doaj.art-43f3c106976744fe9506a0c00ea0cded |
| institution | Directory Open Access Journal |
| issn | 2218-273X |
| language | English |
| last_indexed | 2024-03-10T22:59:11Z |
| publishDate | 2023-09-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Biomolecules |
| spelling | doaj.art-43f3c106976744fe9506a0c00ea0cded2023-11-19T09:46:42ZengMDPI AGBiomolecules2218-273X2023-09-01139141910.3390/biom13091419Redox Metabolism and Vascular Calcification in Chronic Kidney DiseaseNatalia Carrillo-López0Sara Panizo1Beatriz Martín-Carro2Juan Carlos Mayo Barrallo3Pablo Román-García4Raúl García-Castro5Jesús María Fernández-Gómez6Miguel Ángel Hevia-Suárez7Julia Martín-Vírgala8Sara Fernández-Villabrille9Laura Martínez-Arias10Sara Barrio Vázquez11Laura Calleros Basilio12Manuel Naves-Díaz13Jorge Benito Cannata-Andía14Isabel Quirós-González15Cristina Alonso-Montes16José Luis Fernández-Martín17Bone and Mineral Research Unit, Instituto de Investigación Sanitaria del Principado de Asturias (ISPA), Hospital Universitario Central de Asturias, 33011 Oviedo, SpainBone and Mineral Research Unit, Instituto de Investigación Sanitaria del Principado de Asturias (ISPA), Hospital Universitario Central de Asturias, 33011 Oviedo, SpainBone and Mineral Research Unit, Instituto de Investigación Sanitaria del Principado de Asturias (ISPA), Hospital Universitario Central de Asturias, 33011 Oviedo, SpainDepartment of Cellular Morphology and Biology, Instituto Universitario de Oncologia del Principado de Asturias (IUOPA), Instituto de Investigación Sanitaria del Principado de Asturias (ISPA), Universidad Oviedo, 33006 Oviedo, SpainBone and Mineral Research Unit, Instituto de Investigación Sanitaria del Principado de Asturias (ISPA), Hospital Universitario Central de Asturias, 33011 Oviedo, SpainDepartment of Nephrology, Hospital Juaneda Miramar, Red Asistencial Juaneda, 07011 Palma de Mallorca, SpainUGC of Urology, Hospital Universitario Central de Asturias, Universidad de Oviedo, 33011 Oviedo, SpainUGC of Urology, Hospital Universitario Central de Asturias, Universidad de Oviedo, 33011 Oviedo, SpainBone and Mineral Research Unit, Instituto de Investigación Sanitaria del Principado de Asturias (ISPA), Hospital Universitario Central de Asturias, 33011 Oviedo, SpainBone and Mineral Research Unit, Instituto de Investigación Sanitaria del Principado de Asturias (ISPA), Hospital Universitario Central de Asturias, 33011 Oviedo, SpainBone and Mineral Research Unit, Instituto de Investigación Sanitaria del Principado de Asturias (ISPA), Hospital Universitario Central de Asturias, 33011 Oviedo, SpainBone and Mineral Research Unit, Instituto de Investigación Sanitaria del Principado de Asturias (ISPA), Hospital Universitario Central de Asturias, 33011 Oviedo, SpainRedes de Investigación Cooperativa Orientadas a Resultados en Salud (RICORS), RICORS2040 (Kidney Disease), 28029 Madrid, SpainBone and Mineral Research Unit, Instituto de Investigación Sanitaria del Principado de Asturias (ISPA), Hospital Universitario Central de Asturias, 33011 Oviedo, SpainBone and Mineral Research Unit, Instituto de Investigación Sanitaria del Principado de Asturias (ISPA), Hospital Universitario Central de Asturias, 33011 Oviedo, SpainDepartment of Cellular Morphology and Biology, Instituto Universitario de Oncologia del Principado de Asturias (IUOPA), Instituto de Investigación Sanitaria del Principado de Asturias (ISPA), Universidad Oviedo, 33006 Oviedo, SpainBone and Mineral Research Unit, Instituto de Investigación Sanitaria del Principado de Asturias (ISPA), Hospital Universitario Central de Asturias, 33011 Oviedo, SpainBone and Mineral Research Unit, Instituto de Investigación Sanitaria del Principado de Asturias (ISPA), Hospital Universitario Central de Asturias, 33011 Oviedo, SpainVascular calcification (VC) is a common complication in patients with chronic kidney disease which increases their mortality. Although oxidative stress is involved in the onset and progression of this disorder, the specific role of some of the main redox regulators, such as catalase, the main scavenger of H<sub>2</sub>O<sub>2</sub>, remains unclear. In the present study, epigastric arteries of kidney transplant recipients, a rat model of VC, and an in vitro model of VC exhibiting catalase (Cts) overexpression were analysed. Pericalcified areas of human epigastric arteries had increased levels of catalase and cytoplasmic, rather than nuclear runt-related transcription factor 2 (RUNX2). In the rat model, advanced aortic VC concurred with lower levels of the H<sub>2</sub>O<sub>2</sub>-scavenger glutathione peroxidase 3 compared to controls. In an early model of calcification using vascular smooth muscle cells (VSMCs), Cts VSMCs showed the expected increase in total levels of RUNX2. However, Cts VMSCs also exhibited a lower percentage of the nucleus stained for RUNX2 in response to calcifying media. In this early model of VC, we did not observe a dysregulation of the mitochondrial redox state; instead, an increase in the general redox state was observed in the cytoplasm. These results highlight the complex role of antioxidant enzymes as catalase by regulation of RUNX2 subcellular location delaying the onset of VC.https://www.mdpi.com/2218-273X/13/9/1419vascular calcificationcatalaseCKDRUNX2epigastric arteriesDIGE |
| spellingShingle | Natalia Carrillo-López Sara Panizo Beatriz Martín-Carro Juan Carlos Mayo Barrallo Pablo Román-García Raúl García-Castro Jesús María Fernández-Gómez Miguel Ángel Hevia-Suárez Julia Martín-Vírgala Sara Fernández-Villabrille Laura Martínez-Arias Sara Barrio Vázquez Laura Calleros Basilio Manuel Naves-Díaz Jorge Benito Cannata-Andía Isabel Quirós-González Cristina Alonso-Montes José Luis Fernández-Martín Redox Metabolism and Vascular Calcification in Chronic Kidney Disease Biomolecules vascular calcification catalase CKD RUNX2 epigastric arteries DIGE |
| title | Redox Metabolism and Vascular Calcification in Chronic Kidney Disease |
| title_full | Redox Metabolism and Vascular Calcification in Chronic Kidney Disease |
| title_fullStr | Redox Metabolism and Vascular Calcification in Chronic Kidney Disease |
| title_full_unstemmed | Redox Metabolism and Vascular Calcification in Chronic Kidney Disease |
| title_short | Redox Metabolism and Vascular Calcification in Chronic Kidney Disease |
| title_sort | redox metabolism and vascular calcification in chronic kidney disease |
| topic | vascular calcification catalase CKD RUNX2 epigastric arteries DIGE |
| url | https://www.mdpi.com/2218-273X/13/9/1419 |
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