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Article

A Dual Role of Heme Oxygenase-1 in Angiotensin II-Induced Abdominal Aortic Aneurysm in the Normolipidemic Mice

1
Department of Medical Biotechnology, Faculty of Biochemistry, Biophysics and Biotechnology, Jagiellonian University, 30-392 Krakow, Poland
2
Department of Animal Reproduction, Anatomy and Genomic, Faculty of Animal Science, University of Agriculture, 30-059 Krakow, Poland
*
Author to whom correspondence should be addressed.
Cells 2021, 10(1), 163; https://doi.org/10.3390/cells10010163
Received: 15 December 2020 / Revised: 9 January 2021 / Accepted: 12 January 2021 / Published: 15 January 2021
(This article belongs to the Special Issue New Insight into Heme Oxygenases: Beyond Heme Degradation)
Abdominal aortic aneurysm (AAA) bears a high risk of rupture and sudden death of the patient. The pathogenic mechanisms of AAA remain elusive, and surgical intervention represents the only treatment option. Heme oxygenase-1 (HO-1), a heme degrading enzyme, is induced in AAA, both in mice and humans. HO-1 was reported to mitigate AAA development in an angiotensin II (AngII)-induced model of AAA in hyperlipidemic ApoE-/- mice. Since the role of hyperlipidaemia in the pathogenesis of AAA remains controversial, we aimed to evaluate the significance of HO-1 in the development and progression of AAA in normolipidemic animals. The experiments were performed in HO-1-deficient mice and their wild-type counterparts. We demonstrated in non-hypercholesterolemic mice that the high-dose of AngII leads to the efficient formation of AAA, which is attenuated by HO-1 deficiency. Yet, if formed, they are significantly more prone to rupture upon HO-1 shortage. Differential susceptibility to AAA formation does not rely on enhanced inflammatory response or oxidative stress. AAA-resistant mice are characterized by an increase in regulators of aortic remodeling and angiotensin receptor-2 expression, significant medial thickening, and delayed blood pressure elevation in response to AngII. To conclude, we unveil a dual role of HO-1 deficiency in AAA in normolipidemic mice, where it protects against AAA development, but exacerbates the state of formed AAA. View Full-Text
Keywords: heme oxygenase 1; HO-1; abdominal aortic aneurysm; AAA; cardiovascular system; angiotensin II heme oxygenase 1; HO-1; abdominal aortic aneurysm; AAA; cardiovascular system; angiotensin II
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MDPI and ACS Style

Kopacz, A.; Klóska, D.; Werner, E.; Hajduk, K.; Grochot-Przęczek, A.; Józkowicz, A.; Piechota-Polańczyk, A. A Dual Role of Heme Oxygenase-1 in Angiotensin II-Induced Abdominal Aortic Aneurysm in the Normolipidemic Mice. Cells 2021, 10, 163. https://doi.org/10.3390/cells10010163

AMA Style

Kopacz A, Klóska D, Werner E, Hajduk K, Grochot-Przęczek A, Józkowicz A, Piechota-Polańczyk A. A Dual Role of Heme Oxygenase-1 in Angiotensin II-Induced Abdominal Aortic Aneurysm in the Normolipidemic Mice. Cells. 2021; 10(1):163. https://doi.org/10.3390/cells10010163

Chicago/Turabian Style

Kopacz, Aleksandra, Damian Klóska, Ewa Werner, Karolina Hajduk, Anna Grochot-Przęczek, Alicja Józkowicz, and Aleksandra Piechota-Polańczyk. 2021. "A Dual Role of Heme Oxygenase-1 in Angiotensin II-Induced Abdominal Aortic Aneurysm in the Normolipidemic Mice" Cells 10, no. 1: 163. https://doi.org/10.3390/cells10010163

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