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  • 51.
    Wågsäter, Dick
    et al.
    Karolinska University hospital, Karolinska Institutet, Stockholm, Sweden .
    Paloschi, Valentina
    Karolinska University hospital, Karolinska Institutet, Stockholm, Sweden .
    Hanemaaijer, Roeland
    TNO Metabolic Health Research, Leiden, the Netherlands .
    Hultenby, Kjell
    Karolinska Institutet, Stockholm, Sweden.
    Bank, Ruud A
    University Medical Center Groningen, the Netherlands .
    Franco-Cereceda, Anders
    Karolinska Institutet, Stockholm, Sweden.
    Lindeman, Jan H N
    Leiden University Medical Center, the Netherlands .
    Eriksson, Per
    Karolinska University hospital, Karolinska Institutet, Stockholm, Sweden .
    Impaired collagen biosynthesis and cross-linking in aorta of patients with bicuspid aortic valve2013In: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease, ISSN 2047-9980, E-ISSN 2047-9980, Vol. 2, no 1, p. e000034-Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Patients with bicuspid aortic valve (BAV) have an increased risk of developing ascending aortic aneurysm. In the present study, collagen homeostasis in nondilated and dilated aorta segments from patients with BAV was studied, with normal and dilated aortas from tricuspid aortic valve (TAV) patients as reference.

    METHODS AND RESULTS: Ascending aortas from 56 patients were used for biochemical and morphological analyses of collagen. mRNA expression was analyzed in 109 patients. Collagen turnover rates were similar in nondilated and dilated aortas of BAV patients, showing that aneurysmal formation in BAV is, in contrast to TAV, not associated with an increased collagen turnover. However, BAV in general was associated with an increased aortic collagen turnover compared with nondilated aortas of TAV patients. Importantly, the ratio of hydroxylysyl pyridinoline (HP) to lysyl pyridinoline (LP), 2 distinct forms of collagen cross-linking, was lower in dilated aortas from patients with BAV, which suggests that BAV is associated with a defect in the posttranslational collagen modification. This suggests a deficiency at the level of lysyl hydroxylase (PLOD1), which was confirmed by mRNA and protein analyses that showed reduced PLOD1 expression but normal lysyl oxidase expression in dilated aortas from patients with BAV. This suggests that impaired collagen cross-linking in BAV patients may be attributed to changes in the expression and/or activity of PLOD1.

    CONCLUSIONS: Our results demonstrate an impaired biosynthesis and posttranslational modification of collagen in aortas of patients with BAV, which may explain the increased aortic aneurysm formation in BAV patients.

  • 52.
    Wågsäter, Dick
    et al.
    University of Örebro, Sweden.
    Sheikine, Y
    University of Örebro, Sweden.
    Sirsjö, A
    University of Örebro, Sweden.
    All-trans retinoic acid regulates CXCL16/SR-PSOX expression2005In: International Journal of Molecular Medicine, ISSN 1107-3756, E-ISSN 1791-244X, Vol. 16, no 4, p. 661-665Article in journal (Refereed)
    Abstract [en]

    Several studies have shown the ability of retinoids to modulate inflammatory response. CXCL16/SR-PSOX is a novel protein functioning as a chemokine and a scavenger receptor. We investigated effects of all-trans retinoic acid (atRA) on CXCL16/SR-PSOX expression in several cell types. Real-time PCR showed that atRA increased CXCL16/SRPSOX mRNA expression in THP-1 and endothelial cells, which corresponded to increased release of CXCL16 protein from the cells, measured by ELISA. In THP-1 cells this effect was reduced by retinoic acid receptor (RAR) antagonist, which indicates receptor-mediated inhibition. RAR-alpha and RAR-gamma agonists increased CXCL16 release, which suggests RAR-mediated effect of atRA, which is not selective for a particular RAR subtype. In smooth muscle cells, up-regulation of CXCL16 mRNA was observed only after 96 h of treatment, while protein expression did not change. These findings suggest that retinoid signaling might be a pathway modulating inflammatory response by regulating CXCL16 expression in a cell-specific manner.

  • 53.
    Wågsäter, Dick
    et al.
    University of Örebro, Sweden.
    Sirsjö, Allan
    University of Örebro, Sweden.
    Dimberg, Jan
    School of Health Sciences, Jönköping; Sweden.
    Down-regulation of ID2 by all-trans retinoic acid in monocytic leukemia cells (THP-1)2003In: Journal of Experimental and Clinical Cancer Research, ISSN 1756-9966, E-ISSN 1756-9966, Vol. 22, no 3, p. 471-475Article in journal (Refereed)
    Abstract [en]

    Accumulated evidence supports that both Id helix-loop-helix proteins and derivatives of vitamin A, retinoids, play a pivotal role in the regulation of cell growth and differentiation. We analyzed the effects of all-trans retinoic acid (atRA) on the gene and protein expression of Id2 in THP-1 cells and found a suppression of the levels of Id2. The down-regulation was abolished towards a constitutively expressed level of Id2 mRNA. The decreased level of Id2 was associated with growth suppression and does support the prevalent conception of the action of Id2 as a stimulator of cell growth.

  • 54.
    Wågsäter, Dick
    et al.
    Karolinska Institute, Solna, Stockholm, Sweden.
    Zhu, Chaoyong
    Karolinska Institute, Solna, Stockholm, Sweden.
    Björkegren, Johan
    Karolinska Institute, Solna, Stockholm, Sweden.
    Skogsberg, Josefin
    Karolinska Institute, Solna, Stockholm, Sweden.
    Eriksson, Per
    Karolinska Institute, Solna, Stockholm, Sweden.
    MMP-2 and MMP-9 are prominent matrix metalloproteinases during atherosclerosis development in the LdlrApob100/100 mouse2011In: International Journal of Molecular Medicine, ISSN 1107-3756, E-ISSN 1791-244X, Vol. 28, no 2, p. 247-253Article in journal (Refereed)
    Abstract [en]

    Matrix-degrading proteases capable of degrading components of the extracellular matrix may play an important role in development and progression of atherosclerotic lesions. In the present study, we used the Ldlr(-/-)Apob(100/100) mouse model, which has a plasma lipoprotein profile similar to that of humans with atherosclerosis, to study the expression of matrix metalloproteinases (MMPs) during early stages of atherosclerosis development. We analyzed the expression of 11 proteases and three protease inhibitors in 5- to 40-week-old Ldlr(-/-)Apob(100/100) mice. Expression and activity of MMP-2 and MMP-9 was increased in advanced atherosclerotic lesions followed by macrophage infiltration as shown by real-time PCR, gel-based and in situ zymography and immunohistochemistry. Expression of other investigated MMPs did not increase during disease progression. However, the mRNA expression of MMP-8 and MMP-13 was down-regulated, which could explain the relatively high amount of collagen observed in the vessels in this model. In conclusion, low proteolytic expression at early stages of atherogenesis and a limited repertoire of proteolytic enzymes were associated with the progression of atherosclerosis in Ldlr(-/-)Apob(100/100) mice. The study suggests that MMP-2 and MMP-9 are the main proteases involved in atherogenesis in this mouse model.

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