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- Rattik, Sara, et al.
(författare)
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IL-22 affects smooth muscle cell phenotype and plaque formation in apolipoprotein E knockout mice.
- 2015
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Ingår i: Atherosclerosis. - : Elsevier BV. - 1879-1484 .- 0021-9150. ; 242:2, s. 506-514
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Tidskriftsartikel (refereegranskat)abstract
- IL-22 is a recently discovered cytokine that belongs to the family of IL-10 related cytokines. It is produced by activated T-cells and innate lymphoid cells and has been suggested to be involved in tissue repair. As both inflammation and repair play important roles in atherosclerosis we investigated if IL-22 deficiency influences the disease process in Apoe(-/-) mice.
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2. |
- Rauch, Uwe, et al.
(författare)
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Laminin isoforms in atherosclerotic arteries from mice and man.
- 2011
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Ingår i: Histology and Histopathology. - 1699-5848. ; 26:6, s. 711-724
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Tidskriftsartikel (refereegranskat)abstract
- The properties of the arterial vasculature depend to a large extent on the activities of smooth muscle cells, which, in turn, are determined by their extracellular environment. During pathological conditions, such as atherosclerosis, this interaction is altered. In close proximity to medial smooth muscle cells are basement membrane components, such as different isoforms of laminin. These proteins can have great impact on cellular function via interaction with cell surface integrins. However, knowledge of laminins in smooth muscle cell basement membranes during normal and pathological conditions is scarce. Therefore, we have analyzed the presence of laminin isoforms in atherosclerotic lesions of apolipoprotein E (ApoE)-deficient mice. Our study revealed that the laminin chain isotype composition within atherosclerotic plaque tissue was different from the chain composition in the media. In addition, obvious differences in laminin chain composition could be observed in areas of the media, which were or were not associated with plaque tissue. Our major findings demonstrate that laminin gamma3 was exclusively present in media associated with plaque tissue. Laminin alpha2 was also enriched in these medial areas. Plaque tissue was predominantly enriched in laminin alpha5 chains. This general distribution applied to lesions both with and without a fibrous cap-like structure. The differential distribution of laminin chains were partially accompanied by changes in the presence of the integrin alpha subunits 7 and V. The distribution of laminin chains in human atherosclerotic arteries, with different size and morphology, grossly resembled their distribution in mouse arteries.
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3. |
- Saxena, Amit, et al.
(författare)
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The Vascular Repair Process after Injury of the Carotid Artery is regulated by IL-1RI and MyD88 Signalling.
- 2011
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Ingår i: Cardiovascular Research. - : Oxford University Press (OUP). - 1755-3245 .- 0008-6363. ; 91, s. 350-357
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Tidskriftsartikel (refereegranskat)abstract
- Aim: The aim of this study was to determine if innate immune signalling influences the vascular repair process in response to mechanical injury of arteries in mice. Methods and Results: A non-obstructive collar was introduced around the carotid artery of MyD88-deficient mice and neointima formation was compared to that observed in MyD88-competent mice. MyD88-deficient mice are characterized by impaired signal transduction from interleukin (IL)-1/IL-18 receptors and most Toll-like receptors. The vascular response to injury was severely impaired in MyD88-deficient mice as neointima formation was not different from sham operated mice, whereas MyD88-competent mice displayed robust neointima formation. Furthermore, infiltration of CD68 positive leukocytes was dependent on MyD88. During the early response to injury, 3 days after collar placement, a transient increase in the expression of Toll-like receptor (TLR) 4 on vascular smooth muscle cells was observed. To determine the relative importance of IL-1 receptor and TLR4 activation in the vascular response to injury mice were injected with blocking antibodies to these receptors prior to the collar placement. Neointima formation was reduced by 80% in mice administered IL-1RI blocking antibodies compared to mice given a control antibody, whereas administration of TLR4 blocking antibodies was without effect. Conclusion: These results show that inhibition of MyD88- or IL-1 receptor signalling reduces neointima formation in response to vascular injury and could offer therapeutic options for reducing clinical complications of excessive smooth muscle cell proliferation, such as that observed in in-stent restenosis.
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