MYD88 and Proinflammatory Chemokines in Aortic Atheromatosis: Exploring Novel Statin Effects

Atherosclerosis is driven by a diverse range of cellular and molecular processes. In the present study, we sought to better understand how statins mitigate proatherogenic inflammation. 48 male New Zealand rabbits were divided into eight groups, each including 6 animals. The control groups received n...

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Main Authors: Konstantinos S. Mylonas, Michail Peroulis, Dimitrios Schizas, Alkistis Kapelouzou
Format: Article
Language:English
Published: MDPI AG 2023-05-01
Series:International Journal of Molecular Sciences
Subjects:
Online Access:https://www.mdpi.com/1422-0067/24/11/9248
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author Konstantinos S. Mylonas
Michail Peroulis
Dimitrios Schizas
Alkistis Kapelouzou
author_facet Konstantinos S. Mylonas
Michail Peroulis
Dimitrios Schizas
Alkistis Kapelouzou
author_sort Konstantinos S. Mylonas
collection DOAJ
description Atherosclerosis is driven by a diverse range of cellular and molecular processes. In the present study, we sought to better understand how statins mitigate proatherogenic inflammation. 48 male New Zealand rabbits were divided into eight groups, each including 6 animals. The control groups received normal chow for 90 and 120 days. Three groups underwent a hypercholesterolemic diet (HCD) for 30, 60, and 90 days. Another three groups underwent HCD for 3 months, followed by normal chow for one month, with or without rosuvastatin or fluvastatin. The cytokine and chemokine expressions were assessed in the samples of thoracic and abdominal aorta. Rosuvastatin significantly reduced MYD88, CCL4, CCL20, CCR2, TNF-α, IFN-β, IL-1b, IL-2, IL-4, IL-8, and IL-10, both in the thoracic and abdominal aorta. Fluvastatin also downregulated MYD88, CCR2, IFN-β, IFN-γ, IL-1b, IL-2, IL-4, and IL-10 in both aortic segments. Rosuvastatin curtailed the expression of CCL4, IFN-β, IL-2, IL-4, and IL-10 more effectively than fluvastatin in both types of tissue. MYD88, TNF-α, IL-1b, and IL-8 showed a stronger downregulation with rosuvastatin compared to fluvastatin only in the thoracic aorta. The CCL20 and CCR2 levels reduced more extensively with rosuvastatin treatment only in abdominal aortic tissue. In conclusion, statin therapy can halt proatherogenic inflammation in hyperlipidemic animals. Rosuvastatin may be more effective in downregulating MYD88 in atherosclerotic thoracic aortas.
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spelling doaj.art-f435579aa32741f5ba5977d56d79789c2023-11-18T07:56:24ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672023-05-012411924810.3390/ijms24119248MYD88 and Proinflammatory Chemokines in Aortic Atheromatosis: Exploring Novel Statin EffectsKonstantinos S. Mylonas0Michail Peroulis1Dimitrios Schizas2Alkistis Kapelouzou3Department of Cardiac Surgery, Onassis Cardiac Surgery Center, 176 71 Athens, GreeceVascular Surgery Unit, Department of Surgery, Faculty of Medicine, University of Ioannina, 451 10 Ioannina, GreeceFirst Department of Cardiac Surgery, Laikon General Hospital, National and Kapodistrian University of Athens, 176 71 Athens, GreeceClinical, Experimental Surgery & Translational Research, Biomedical Research Foundation Academy of Athens, 176 71 Athens, GreeceAtherosclerosis is driven by a diverse range of cellular and molecular processes. In the present study, we sought to better understand how statins mitigate proatherogenic inflammation. 48 male New Zealand rabbits were divided into eight groups, each including 6 animals. The control groups received normal chow for 90 and 120 days. Three groups underwent a hypercholesterolemic diet (HCD) for 30, 60, and 90 days. Another three groups underwent HCD for 3 months, followed by normal chow for one month, with or without rosuvastatin or fluvastatin. The cytokine and chemokine expressions were assessed in the samples of thoracic and abdominal aorta. Rosuvastatin significantly reduced MYD88, CCL4, CCL20, CCR2, TNF-α, IFN-β, IL-1b, IL-2, IL-4, IL-8, and IL-10, both in the thoracic and abdominal aorta. Fluvastatin also downregulated MYD88, CCR2, IFN-β, IFN-γ, IL-1b, IL-2, IL-4, and IL-10 in both aortic segments. Rosuvastatin curtailed the expression of CCL4, IFN-β, IL-2, IL-4, and IL-10 more effectively than fluvastatin in both types of tissue. MYD88, TNF-α, IL-1b, and IL-8 showed a stronger downregulation with rosuvastatin compared to fluvastatin only in the thoracic aorta. The CCL20 and CCR2 levels reduced more extensively with rosuvastatin treatment only in abdominal aortic tissue. In conclusion, statin therapy can halt proatherogenic inflammation in hyperlipidemic animals. Rosuvastatin may be more effective in downregulating MYD88 in atherosclerotic thoracic aortas.https://www.mdpi.com/1422-0067/24/11/9248MYD88CCL4CCL20CCR2atherosclerosisstatin
spellingShingle Konstantinos S. Mylonas
Michail Peroulis
Dimitrios Schizas
Alkistis Kapelouzou
MYD88 and Proinflammatory Chemokines in Aortic Atheromatosis: Exploring Novel Statin Effects
International Journal of Molecular Sciences
MYD88
CCL4
CCL20
CCR2
atherosclerosis
statin
title MYD88 and Proinflammatory Chemokines in Aortic Atheromatosis: Exploring Novel Statin Effects
title_full MYD88 and Proinflammatory Chemokines in Aortic Atheromatosis: Exploring Novel Statin Effects
title_fullStr MYD88 and Proinflammatory Chemokines in Aortic Atheromatosis: Exploring Novel Statin Effects
title_full_unstemmed MYD88 and Proinflammatory Chemokines in Aortic Atheromatosis: Exploring Novel Statin Effects
title_short MYD88 and Proinflammatory Chemokines in Aortic Atheromatosis: Exploring Novel Statin Effects
title_sort myd88 and proinflammatory chemokines in aortic atheromatosis exploring novel statin effects
topic MYD88
CCL4
CCL20
CCR2
atherosclerosis
statin
url https://www.mdpi.com/1422-0067/24/11/9248
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