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Article ; Online: Acetylsalicylic Acid Reduces Passive Aortic Wall Stiffness and Cardiovascular Remodelling in a Mouse Model of Advanced Atherosclerosis

Lynn Roth / Miche Rombouts / Dorien M. Schrijvers / Besa Emini Veseli / Wim Martinet / Guido R. Y. De Meyer

International Journal of Molecular Sciences, Vol 23, Iss 404, p

2022 Volume 404

Abstract: Acetylsalicylic acid (ASA) is widely used in secondary prevention of cardiovascular (CV) disease, mainly because of its antithrombotic effects. Here, we investigated whether ASA can prevent the progression of vessel wall remodelling, atherosclerosis, and ...

Abstract	Acetylsalicylic acid (ASA) is widely used in secondary prevention of cardiovascular (CV) disease, mainly because of its antithrombotic effects. Here, we investigated whether ASA can prevent the progression of vessel wall remodelling, atherosclerosis, and CV complications in apolipoprotein E deficient ( ApoE −/− ) mice, a model of stable atherosclerosis, and in ApoE −/− mice with a mutation in the fibrillin-1 gene ( Fbn1 C1039G+/− ), which is a model of elastic fibre fragmentation, accompanied by exacerbated unstable atherosclerosis. Female ApoE −/− and ApoE −/− Fbn1 C1039G+/− mice were fed a Western diet (WD). At 10 weeks of WD, the mice were randomly divided into four groups, receiving either ASA 5 mg/kg/day in the drinking water ( ApoE −/− ( n = 14), ApoE −/− Fbn1 C1039G+/− ( n = 19)) or plain drinking water ( ApoE −/− ( n = 15), ApoE −/− Fbn1 C1039G+/− ( n = 21)) for 15 weeks. ApoE −/− Fbn1 C1039G+/− mice showed an increased neutrophil–lymphocyte ratio (NLR) compared to ApoE −/− mice, and this effect was normalised by ASA. In the proximal ascending aorta wall, ASA-treated ApoE −/− Fbn1 C1039G+/− mice showed less p-SMAD2/3 positive nuclei, a lower collagen percentage and an increased elastin/collagen ratio, consistent with the values measured in ApoE −/− mice. ASA did not affect plaque progression, incidence of myocardial infarction and survival of ApoE −/− Fbn1 C1039G+/− mice, but systolic blood pressure, cardiac fibrosis and hypertrophy were reduced. In conclusion, ASA normalises the NLR, passive wall stiffness and cardiac remodelling in ApoE −/− Fbn1 C1039G+/− mice to levels observed in ApoE −/− mice, indicating additional therapeutic benefits of ASA beyond its classical use.
Keywords	arterial stiffness ; neutrophil–lymphocyte ratio ; collagen ; SMAD ; elastin ; aspirin ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Language	English
Publishing date	2022-12-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
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Article ; Online: Acetylsalicylic Acid Reduces Passive Aortic Wall Stiffness and Cardiovascular Remodelling in a Mouse Model of Advanced Atherosclerosis.

Roth, Lynn / Rombouts, Miche / Schrijvers, Dorien M / Emini Veseli, Besa / Martinet, Wim / De Meyer, Guido R Y

International journal of molecular sciences

2021 Volume 23, Issue 1

Abstract	Acetylsalicylic acid (ASA) is widely used in secondary prevention of cardiovascular (CV) disease, mainly because of its antithrombotic effects. Here, we investigated whether ASA can prevent the progression of vessel wall remodelling, atherosclerosis, and CV complications in apolipoprotein E deficient (
MeSH term(s)	Animals ; Aorta/drug effects ; Aorta/pathology ; Aorta/physiopathology ; Apolipoproteins E/deficiency ; Apolipoproteins E/metabolism ; Aspirin/pharmacology ; Atherosclerosis/pathology ; Atherosclerosis/physiopathology ; Blood Pressure/drug effects ; Disease Models, Animal ; Disease Progression ; Female ; Fibrillin-1/metabolism ; Kaplan-Meier Estimate ; Lymphocytes/drug effects ; Lymphocytes/metabolism ; Mice ; Myocardial Infarction/physiopathology ; Neutrophils/drug effects ; Neutrophils/metabolism ; Vascular Remodeling/drug effects ; Vascular Stiffness/drug effects
Chemical Substances	Apolipoproteins E ; Fibrillin-1 ; Aspirin (R16CO5Y76E)
Language	English
Publishing date	2021-12-30
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms23010404
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Article ; Online: MicroRNA-216a is essential for cardiac angiogenesis.

Juni, Rio P / Kocken, Jordy M M / Abreu, Ricardo C / Ottaviani, Lara / Davalan, Tim / Duygu, Burcu / Poels, Ella M / Vasilevich, Aliaksei / Hegenbarth, Jana C / Appari, Mahesh / Bitsch, Nicole / Olieslagers, Serve / Schrijvers, Dorien M / Stoll, Monika / Heineke, Joerg / de Boer, Jan / de Windt, Leon J / da Costa Martins, Paula A

Molecular therapy : the journal of the American Society of Gene Therapy

2023 Volume 31, Issue 6, Page(s) 1807–1828

Abstract: While it is experimentally supported that impaired myocardial vascularization contributes to a mismatch between myocardial oxygen demand and supply, a mechanistic basis for disruption of coordinated tissue growth and angiogenesis in heart failure remains ...

Abstract	While it is experimentally supported that impaired myocardial vascularization contributes to a mismatch between myocardial oxygen demand and supply, a mechanistic basis for disruption of coordinated tissue growth and angiogenesis in heart failure remains poorly understood. Silencing strategies that impair microRNA biogenesis have firmly implicated microRNAs in the regulation of angiogenesis, and individual microRNAs prove to be crucial in developmental or tumor angiogenesis. A high-throughput functional screening for the analysis of a whole-genome microRNA silencing library with regard to their phenotypic effect on endothelial cell proliferation as a key parameter, revealed several anti- and pro-proliferative microRNAs. Among those was miR-216a, a pro-angiogenic microRNA which is enriched in cardiac microvascular endothelial cells and reduced in expression under cardiac stress conditions. miR-216a null mice display dramatic cardiac phenotypes related to impaired myocardial vascularization and unbalanced autophagy and inflammation, supporting a model where microRNA regulation of microvascularization impacts the cardiac response to stress.
MeSH term(s)	Animals ; Mice ; Endothelial Cells/metabolism ; Heart Failure/metabolism ; MicroRNAs/metabolism ; Myocardium/metabolism ; Neovascularization, Pathologic/genetics ; Neovascularization, Pathologic/metabolism ; Neovascularization, Physiologic/genetics
Chemical Substances	MicroRNAs ; MIRN216 microRNA, mouse
Language	English
Publishing date	2023-04-17
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2010592-7
ISSN	1525-0024 ; 1525-0016
ISSN (online)	1525-0024
ISSN	1525-0016
DOI	10.1016/j.ymthe.2023.04.007
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Article ; Online: Defective Autophagy in Atherosclerosis: To Die or to Senesce?

Grootaert, Mandy O J / Roth, Lynn / Schrijvers, Dorien M / De Meyer, Guido R Y / Martinet, Wim

Oxidative medicine and cellular longevity

2018 Volume 2018, Page(s) 7687083

Abstract: Autophagy is a subcellular process that plays an important role in the degradation of proteins and damaged organelles such as mitochondria (a process termed "mitophagy") via lysosomes. It is crucial for regulating protein and mitochondrial quality ... ...

Abstract	Autophagy is a subcellular process that plays an important role in the degradation of proteins and damaged organelles such as mitochondria (a process termed "mitophagy") via lysosomes. It is crucial for regulating protein and mitochondrial quality control and maintaining cellular homeostasis, whereas dysregulation of autophagy has been implicated in a wide range of diseases including atherosclerosis. Recent evidence has shown that the autophagic process becomes dysfunctional during the progression of atherosclerosis, regardless of whether there are many autophagy-stimulating factors (e.g., reactive oxygen species, oxidized lipids, and cytokines) present within the atherosclerotic plaque. This review highlights the recent insights into the causes and consequences of defective autophagy in atherosclerosis, with a special focus on the role of autophagy and mitophagy in plaque macrophages, vascular smooth muscle cells (VSMCs), and endothelial cells (ECs). It has been shown that defective autophagy can promote apoptosis in macrophages but that it accelerates premature senescence in VSMCs. In the ECs, defective autophagy promotes both apoptosis and senescence. We will discuss the discrepancy between these three cell types in their response to autophagy deficiency and underline the cell type-dependent role of autophagy, which may have important implications for the efficacy of autophagy-targeted treatments for atherosclerosis.
MeSH term(s)	Animals ; Apoptosis/physiology ; Atherosclerosis/metabolism ; Atherosclerosis/physiopathology ; Autophagy/physiology ; Cellular Senescence/physiology ; Humans ; Mitochondrial Degradation/physiology
Language	English
Publishing date	2018-02-26
Publishing country	United States
Document type	Journal Article ; Review
ISSN	1942-0994
ISSN (online)	1942-0994
DOI	10.1155/2018/7687083
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Article: Does patient-tailored immunotherapy pave the way for new renal cell carcinoma treatment perspectives?

Van Brussel, Ilse / Van Craenenbroeck, Amaryllis H / Schrijvers, Dorien M / Cools, Nathalie

Translational andrology and urology

2016 Volume 2, Issue 2, Page(s) 85–88

Language	English
Publishing date	2016-01-01
Publishing country	China
Document type	Journal Article
ZDB-ID	2851630-8
ISSN	2223-4691 ; 2223-4691 ; 2223-4683
ISSN (online)	2223-4691
ISSN	2223-4691 ; 2223-4683
DOI	10.3978/j.issn.2223-4683.2012.10.02
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Article ; Online: Cholesterol-independent effects of atorvastatin prevent cardiovascular morbidity and mortality in a mouse model of atherosclerotic plaque rupture.

Roth, Lynn / Rombouts, Miche / Schrijvers, Dorien M / Martinet, Wim / De Meyer, Guido R Y

Vascular pharmacology

2016 Volume 80, Page(s) 50–58

Abstract: Because cholesterol-independent effects of statins are difficult to determine in patients, we studied these pleiotropic effects in apolipoprotein E-deficient (ApoE(-/-)) mice with a mutation in the fibrillin-1 gene (Fbn1(C1039G+/-)). These mice develop ... ...

Abstract	Because cholesterol-independent effects of statins are difficult to determine in patients, we studied these pleiotropic effects in apolipoprotein E-deficient (ApoE(-/-)) mice with a mutation in the fibrillin-1 gene (Fbn1(C1039G+/-)). These mice develop exacerbated atherosclerosis and spontaneous plaque ruptures, accompanied by myocardial infarctions (MI) and sudden death. ApoE(-/-)Fbn1(C1039G+/-) mice were fed a Western diet (WD). At week 10 of WD, mice were divided in a control (WD), atorvastatin (10mg/kg/day + WD) and cholesterol withdrawal group (cholW, normal chow). The latter was included to compare the effects of atorvastatin with dietary lipid lowering. Fifteen weeks later, the mice were sacrificed. CholW, but not atorvastatin, reduced plasma cholesterol. Survival increased from 50% to 90% both in cholW and atorvastatin treated mice. CholW as well as atorvastatin treatment increased plaque collagen and fibrous cap thickness, but they did not affect the amount of plaque macrophages and T cells. MMP-2 and MMP-9 activity was significantly lower and the expression of MMP-12, TNF-α and IL-1β was strongly reduced in both treatment groups. Blood monocytes and neutrophils returned to baseline levels (ApoE(-/-) mice before the onset of atherosclerosis). Importantly, atorvastatin but not cholW significantly reduced coronary stenosis (from 50 to 28%) and the occurrence of MI (from 43 to 10%). In conclusion, independent of cholesterol lowering, atorvastatin significantly reduced mortality, plaque vulnerability and inflammation to the same extent as cholW. In addition, atorvastatin but not cholW reduced coronary stenosis and the occurrence of MI. These data unequivocally illustrate the significance of the pleiotropic effects of atorvastatin in the prevention of cardiovascular morbidity and mortality.
MeSH term(s)	Animal Feed ; Animals ; Anticholesteremic Agents/administration & dosage ; Anticholesteremic Agents/therapeutic use ; Apolipoproteins E/genetics ; Atorvastatin Calcium/administration & dosage ; Atorvastatin Calcium/therapeutic use ; Cholesterol/blood ; Cholesterol/deficiency ; Disease Models, Animal ; Female ; Fibrillin-1/genetics ; Hypercholesterolemia/blood ; Hypercholesterolemia/drug therapy ; Hypercholesterolemia/genetics ; Hypercholesterolemia/immunology ; Kaplan-Meier Estimate ; Mice, Knockout ; Plaque, Atherosclerotic/blood ; Plaque, Atherosclerotic/etiology ; Plaque, Atherosclerotic/immunology ; Plaque, Atherosclerotic/prevention & control ; Survival Analysis
Chemical Substances	Anticholesteremic Agents ; Apolipoproteins E ; Fbn1 protein, mouse ; Fibrillin-1 ; Atorvastatin Calcium (48A5M73Z4Q) ; Cholesterol (97C5T2UQ7J)
Language	English
Publishing date	2016-05
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2082846-9
ISSN	1879-3649 ; 1537-1891 ; 1879-3649
ISSN (online)	1879-3649 ; 1537-1891
ISSN	1879-3649
DOI	10.1016/j.vph.2016.01.007
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Zs.A 591: Show issues

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Article ; Online: Caspase-3 Deletion Promotes Necrosis in Atherosclerotic Plaques of ApoE Knockout Mice.

Grootaert, Mandy O J / Schrijvers, Dorien M / Hermans, Marthe / Van Hoof, Viviane O / De Meyer, Guido R Y / Martinet, Wim

Oxidative medicine and cellular longevity

2016 Volume 2016, Page(s) 3087469

Abstract: Apoptosis of macrophages and vascular smooth muscle cells (VSMCs) in advanced atherosclerotic plaques contributes to plaque progression and instability. Caspase-3, a key executioner protease in the apoptotic pathway, has been identified in human and ... ...

Abstract	Apoptosis of macrophages and vascular smooth muscle cells (VSMCs) in advanced atherosclerotic plaques contributes to plaque progression and instability. Caspase-3, a key executioner protease in the apoptotic pathway, has been identified in human and mouse atherosclerotic plaques but its role in atherogenesis is not fully explored. We therefore investigated the impact of caspase-3 deletion on atherosclerosis by crossbreeding caspase-3 knockout (Casp3
MeSH term(s)	Animals ; Apolipoproteins E/deficiency ; Apoptosis ; Caspase 3/metabolism ; Mice ; Mice, Knockout ; Necrosis ; Plaque, Atherosclerotic/metabolism
Chemical Substances	Apolipoproteins E ; Caspase 3 (EC 3.4.22.-)
Language	English
Publishing date	2016
Publishing country	United States
Document type	Journal Article
ISSN	1942-0994
ISSN (online)	1942-0994
DOI	10.1155/2016/3087469
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Article ; Online: Molecular and cellular mechanisms of macrophage survival in atherosclerosis.

Martinet, Wim / Schrijvers, Dorien M / De Meyer, Guido R Y

Basic research in cardiology

2012 Volume 107, Issue 6, Page(s) 297

Abstract: Macrophages play a key role in the initiation and progression of atherosclerotic plaques. Although a significant number of macrophages undergoes cell death during plaque development as a result of atherogenic stressors, advanced plaques are characterized ...

Abstract	Macrophages play a key role in the initiation and progression of atherosclerotic plaques. Although a significant number of macrophages undergoes cell death during plaque development as a result of atherogenic stressors, advanced plaques are characterized by a large macrophage content. Macrophage accumulation is mediated by continuous recruitment of monocytes, reduced emigration of macrophages and poor phagocytosis of dead cells which may trigger secondary necrosis and amplification of plaque inflammation. Moreover, an increasing body of evidence indicates that macrophages have developed several strategies to survive and to proliferate in the adverse environment of an advanced atherosclerotic plaque. Macrophages contain organic molecules or enzymes that provide enhanced antioxidant protection. In addition, synthesis of anti-apoptotic proteins is upregulated and several cellular protection mechanisms such as the unfolded protein response and autophagy are activated in macrophages to promote cellular survival. In this review, we discuss these macrophage survival mechanisms that allow growth and destabilization of advanced atherosclerotic plaques.
MeSH term(s)	Animals ; Antioxidants/metabolism ; Apoptosis Regulatory Proteins/metabolism ; Atherosclerosis/immunology ; Atherosclerosis/metabolism ; Autophagy ; Cell Survival ; Humans ; Lipoproteins, LDL/metabolism ; Macrophages/physiology ; Unfolded Protein Response
Chemical Substances	Antioxidants ; Apoptosis Regulatory Proteins ; Lipoproteins, LDL
Language	English
Publishing date	2012-11
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	189755-x
ISSN	1435-1803 ; 0300-8428 ; 0175-9418
ISSN (online)	1435-1803
ISSN	0300-8428 ; 0175-9418
DOI	10.1007/s00395-012-0297-x
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Article ; Online: Defective autophagy in vascular smooth muscle cells accelerates senescence and promotes neointima formation and atherogenesis.

Grootaert, Mandy Oj / da Costa Martins, Paula A / Bitsch, Nicole / Pintelon, Isabel / De Meyer, Guido Ry / Martinet, Wim / Schrijvers, Dorien M

Autophagy

2015 Volume 11, Issue 11, Page(s) 2014–2032

Abstract: Autophagy is triggered in vascular smooth muscle cells (VSMCs) of diseased arterial vessels. However, the role of VSMC autophagy in cardiovascular disease is poorly understood. Therefore, we investigated the effect of defective autophagy on VSMC survival ...

Abstract	Autophagy is triggered in vascular smooth muscle cells (VSMCs) of diseased arterial vessels. However, the role of VSMC autophagy in cardiovascular disease is poorly understood. Therefore, we investigated the effect of defective autophagy on VSMC survival and phenotype and its significance in the development of postinjury neointima formation and atherosclerosis. Tissue-specific deletion of the essential autophagy gene Atg7 in murine VSMCs (atg7
Language	English
Publishing date	2015-09-22
Publishing country	United States
Document type	Journal Article
ZDB-ID	2454135-7
ISSN	1554-8635 ; 1554-8627
ISSN (online)	1554-8635
ISSN	1554-8627
DOI	10.1080/15548627.2015.1096485
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Zs.A 6741: Show issues

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Article ; Online: Pharmacological modulation of cell death in atherosclerosis: a promising approach towards plaque stabilization?

Martinet, Wim / Schrijvers, Dorien M / De Meyer, Guido R Y

British journal of pharmacology

2011 Volume 164, Issue 1, Page(s) 1–13

Abstract: Despite tremendous advances over the last 15 years in identifying vulnerable atherosclerotic plaques, the incidence of death and disability caused by such lesions still remains the number one health threat in developed countries. Therefore, new systemic ... ...

Abstract	Despite tremendous advances over the last 15 years in identifying vulnerable atherosclerotic plaques, the incidence of death and disability caused by such lesions still remains the number one health threat in developed countries. Therefore, new systemic or focal therapies aimed at decreasing the overall burden of disease, and a change to a more benign phenotype, are needed. Because cell death is a prominent feature of advanced atherosclerotic plaques with a major impact on plaque destabilization, an increasing number of compounds targeting the apoptotic or autophagic machinery in atherosclerosis are being explored, predominantly at the preclinical level. This review will provide an overview of these compounds, with a focus on both inhibition and stimulation of cell death, to prevent acute coronary syndromes and sudden cardiac death.
MeSH term(s)	Animals ; Atherosclerosis/drug therapy ; Atherosclerosis/pathology ; Cell Death/drug effects ; Death, Sudden, Cardiac/prevention & control ; Humans ; Plaque, Atherosclerotic/drug therapy ; Plaque, Atherosclerotic/pathology
Language	English
Publishing date	2011-03-21
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	80081-8
ISSN	1476-5381 ; 0007-1188
ISSN (online)	1476-5381
ISSN	0007-1188
DOI	10.1111/j.1476-5381.2011.01342.x
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