Non-activatable mutant of inhibitor of kappa B kinase α (IKKα) exerts vascular site-specific effects on atherosclerosis in Apoe-deficient mice

IKKα is an important regulator of gene expression. As IKKα kinase inactivity in bone marrow-derived cells does not affect atherosclerosis, we here investigate the impact of a whole body-IKKα kinase inactivity on atherosclerosis. Apolipoprotein E (Apoe)-deficient mice homozygous for an activation-res...

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Veröffentlicht in:Atherosclerosis 2020-01, Vol.292, p.23-30
Hauptverfasser: Tilstam, Pathricia V., Soppert, Josefin, Hemmers, Christian, Harlacher, Eva, Döring, Yvonne, van der Vorst, Emiel P.C., Schulte, Corinna, Alampour-Rajabi, Setareh, Theelen, Wendy, Asare, Yaw, de Winther, Menno P.J., Lawrence, Toby, Bernhagen, Jürgen, Schober, Andreas, Zernecke, Alma, Jankowski, Joachim, Weber, Christian, Noels, Heidi
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container_end_page 30
container_issue
container_start_page 23
container_title Atherosclerosis
container_volume 292
creator Tilstam, Pathricia V.
Soppert, Josefin
Hemmers, Christian
Harlacher, Eva
Döring, Yvonne
van der Vorst, Emiel P.C.
Schulte, Corinna
Alampour-Rajabi, Setareh
Theelen, Wendy
Asare, Yaw
de Winther, Menno P.J.
Lawrence, Toby
Bernhagen, Jürgen
Schober, Andreas
Zernecke, Alma
Jankowski, Joachim
Weber, Christian
Noels, Heidi
description IKKα is an important regulator of gene expression. As IKKα kinase inactivity in bone marrow-derived cells does not affect atherosclerosis, we here investigate the impact of a whole body-IKKα kinase inactivity on atherosclerosis. Apolipoprotein E (Apoe)-deficient mice homozygous for an activation-resistant Ikkα-mutant (IkkαAA/AAApoe−/−) and Ikkα+/+Apoe−/− controls received a Western-type diet. Atherosclerotic lesion size and cellular content were analyzed using histology and immunofluorescence. Vascular protein expression and IKKα kinase activity were quantified by Luminex multiplex immuno-assay and ELISA. A vascular site-specific IKKα expression and kinase activation profile was revealed, with higher total IKKα protein levels in aortic root but increased IKKα phosphorylation, representing activated IKKα, in the aortic arch. This was associated with a vascular site-specific effect of IkkαAA/AA knock-in on atherosclerosis: in the aortic root, IkkαAA/AA knock-in decreased lesion size by 22.0 ± 7.7% (p 
doi_str_mv 10.1016/j.atherosclerosis.2019.10.023
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As IKKα kinase inactivity in bone marrow-derived cells does not affect atherosclerosis, we here investigate the impact of a whole body-IKKα kinase inactivity on atherosclerosis. Apolipoprotein E (Apoe)-deficient mice homozygous for an activation-resistant Ikkα-mutant (IkkαAA/AAApoe−/−) and Ikkα+/+Apoe−/− controls received a Western-type diet. Atherosclerotic lesion size and cellular content were analyzed using histology and immunofluorescence. Vascular protein expression and IKKα kinase activity were quantified by Luminex multiplex immuno-assay and ELISA. A vascular site-specific IKKα expression and kinase activation profile was revealed, with higher total IKKα protein levels in aortic root but increased IKKα phosphorylation, representing activated IKKα, in the aortic arch. This was associated with a vascular site-specific effect of IkkαAA/AA knock-in on atherosclerosis: in the aortic root, IkkαAA/AA knock-in decreased lesion size by 22.0 ± 7.7% (p &lt; 0.01), reduced absolute lesional smooth muscle cell numbers and lowered pro-atherogenic MMP2. In contrast, IkkαAA/AA knock-in increased lesion size in the aortic arch by 43.7 ± 20.1% (p &lt; 0.001), increased the abundance of lesional smooth muscle cells in brachiocephalic artery as main arch side branch and elevated MMP2. A similar profile was observed for MMP3. No effects were observed on necrotic core or collagen deposition in atherosclerotic lesions, nor on absolute lesional macrophage numbers. A non-activatable IKKα kinase differentially affects atherosclerosis in aortic root vs. aortic arch/brachiocephalic artery, associated with a differential vascular IKKα expression and kinase activation profile as well as with a vascular site-dependent impact on lesional smooth muscle cell accumulation and protein expression profiles. [Display omitted] •The degree of vascular IKKα expression and kinase activation differs between aortic root and aortic arch.•Ablation of IKKα kinase activation differentially affects atherosclerosis in aortic root vs. aortic arch.•This is associated with a vascular site-dependent impact on lesional smooth muscle cell accumulation and protein profiles.</description><identifier>ISSN: 0021-9150</identifier><identifier>EISSN: 1879-1484</identifier><identifier>DOI: 10.1016/j.atherosclerosis.2019.10.023</identifier><identifier>PMID: 31733453</identifier><language>eng</language><publisher>Ireland: Elsevier B.V</publisher><subject>Animals ; Apolipoproteins E - deficiency ; Atherosclerosis ; Atherosclerosis - etiology ; Atherosclerosis - metabolism ; I-kappa B Kinase - antagonists &amp; inhibitors ; I-kappa B Kinase - genetics ; I-kappa B Kinase - physiology ; IKK ; IKK alpha kinase ; Life Sciences ; Mice ; Mutation ; NF-kappaB</subject><ispartof>Atherosclerosis, 2020-01, Vol.292, p.23-30</ispartof><rights>2019 Elsevier B.V.</rights><rights>Copyright © 2019 Elsevier B.V. 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As IKKα kinase inactivity in bone marrow-derived cells does not affect atherosclerosis, we here investigate the impact of a whole body-IKKα kinase inactivity on atherosclerosis. Apolipoprotein E (Apoe)-deficient mice homozygous for an activation-resistant Ikkα-mutant (IkkαAA/AAApoe−/−) and Ikkα+/+Apoe−/− controls received a Western-type diet. Atherosclerotic lesion size and cellular content were analyzed using histology and immunofluorescence. Vascular protein expression and IKKα kinase activity were quantified by Luminex multiplex immuno-assay and ELISA. A vascular site-specific IKKα expression and kinase activation profile was revealed, with higher total IKKα protein levels in aortic root but increased IKKα phosphorylation, representing activated IKKα, in the aortic arch. This was associated with a vascular site-specific effect of IkkαAA/AA knock-in on atherosclerosis: in the aortic root, IkkαAA/AA knock-in decreased lesion size by 22.0 ± 7.7% (p &lt; 0.01), reduced absolute lesional smooth muscle cell numbers and lowered pro-atherogenic MMP2. In contrast, IkkαAA/AA knock-in increased lesion size in the aortic arch by 43.7 ± 20.1% (p &lt; 0.001), increased the abundance of lesional smooth muscle cells in brachiocephalic artery as main arch side branch and elevated MMP2. A similar profile was observed for MMP3. No effects were observed on necrotic core or collagen deposition in atherosclerotic lesions, nor on absolute lesional macrophage numbers. 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As IKKα kinase inactivity in bone marrow-derived cells does not affect atherosclerosis, we here investigate the impact of a whole body-IKKα kinase inactivity on atherosclerosis. Apolipoprotein E (Apoe)-deficient mice homozygous for an activation-resistant Ikkα-mutant (IkkαAA/AAApoe−/−) and Ikkα+/+Apoe−/− controls received a Western-type diet. Atherosclerotic lesion size and cellular content were analyzed using histology and immunofluorescence. Vascular protein expression and IKKα kinase activity were quantified by Luminex multiplex immuno-assay and ELISA. A vascular site-specific IKKα expression and kinase activation profile was revealed, with higher total IKKα protein levels in aortic root but increased IKKα phosphorylation, representing activated IKKα, in the aortic arch. This was associated with a vascular site-specific effect of IkkαAA/AA knock-in on atherosclerosis: in the aortic root, IkkαAA/AA knock-in decreased lesion size by 22.0 ± 7.7% (p &lt; 0.01), reduced absolute lesional smooth muscle cell numbers and lowered pro-atherogenic MMP2. In contrast, IkkαAA/AA knock-in increased lesion size in the aortic arch by 43.7 ± 20.1% (p &lt; 0.001), increased the abundance of lesional smooth muscle cells in brachiocephalic artery as main arch side branch and elevated MMP2. A similar profile was observed for MMP3. No effects were observed on necrotic core or collagen deposition in atherosclerotic lesions, nor on absolute lesional macrophage numbers. A non-activatable IKKα kinase differentially affects atherosclerosis in aortic root vs. aortic arch/brachiocephalic artery, associated with a differential vascular IKKα expression and kinase activation profile as well as with a vascular site-dependent impact on lesional smooth muscle cell accumulation and protein expression profiles. [Display omitted] •The degree of vascular IKKα expression and kinase activation differs between aortic root and aortic arch.•Ablation of IKKα kinase activation differentially affects atherosclerosis in aortic root vs. aortic arch.•This is associated with a vascular site-dependent impact on lesional smooth muscle cell accumulation and protein profiles.</abstract><cop>Ireland</cop><pub>Elsevier B.V</pub><pmid>31733453</pmid><doi>10.1016/j.atherosclerosis.2019.10.023</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0003-3620-6775</orcidid><orcidid>https://orcid.org/0000-0003-2996-2652</orcidid><orcidid>https://orcid.org/0000-0003-3053-6984</orcidid><orcidid>https://orcid.org/0000-0003-0967-6122</orcidid></addata></record>
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language eng
recordid cdi_hal_primary_oai_HAL_hal_02998565v1
source MEDLINE; Elsevier ScienceDirect Journals
subjects Animals
Apolipoproteins E - deficiency
Atherosclerosis
Atherosclerosis - etiology
Atherosclerosis - metabolism
I-kappa B Kinase - antagonists & inhibitors
I-kappa B Kinase - genetics
I-kappa B Kinase - physiology
IKK
IKK alpha kinase
Life Sciences
Mice
Mutation
NF-kappaB
title Non-activatable mutant of inhibitor of kappa B kinase α (IKKα) exerts vascular site-specific effects on atherosclerosis in Apoe-deficient mice
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