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Träfflista för sökning "WFRF:(Jeppsson Anders 1960) ;pers:(Lundqvist Annika 1969)"

Sökning: WFRF:(Jeppsson Anders 1960) > Lundqvist Annika 1969

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1.
  • Hermansson, Cecilia, et al. (författare)
  • Reduced expression of NLRP3 and MEFV in human ischemic heart tissue.
  • 2013
  • Ingår i: Biochemical and biophysical research communications. - : Elsevier BV. - 1090-2104 .- 0006-291X. ; 430:1, s. 425-428
  • Tidskriftsartikel (refereegranskat)abstract
    • The innate immune system and, in particular, activation of the multi-protein complex known as the inflammasome complex are involved in ischemic injury in myocardial cells. The nucleotide-binding leucine-rich repeat-containing pyrin receptor 3 (NLRP3) inflammasome has been linked to inflammation and NLRP3 is especially important for increased inflammation in atherosclerosis, which may lead to myocardial infarction. Here we investigated how inflammasome molecules are affected in human ischemic heart tissue. Surprisingly the important member of the inflammasome complex, NLRP3, displayed markedly decreased levels in human ischemic heart tissue compared with non ischemic control heart tissue. However, subsequent gene analysis revealed mutations in NLRP3 in human ischemic heart tissues but not in non-ischemic control tissue. Gene polymorphisms in the NLRP3 inflammasome have been shown to be associated with increased IL-1β and IL-18 production and severe inflammation. The autoinflammatory disorder familial Mediterranean fever (FMF) is associated with decreased expression of the Mediterranean fever gene (MEFV) and increased inflammation. We also observed reduced expression of MEFV in ischemic versus non-ischemic heart tissue. Further analyses showed a mutation in MEFV in human ischemic heart tissue but not in non-ischemic control tissue. Our data show that defects in the inflammasome and associated proteins may be involved in promoting ischemic heart disease.
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2.
  • Klevstig, Martina, et al. (författare)
  • Targeting acid sphingomyelinase reduces cardiac ceramide accumulation in the post-ischemic heart
  • 2016
  • Ingår i: Journal of Molecular and Cellular Cardiology. - : Elsevier BV. - 0022-2828 .- 1095-8584. ; 93, s. 69-72
  • Tidskriftsartikel (refereegranskat)abstract
    • Ceramide accumulation is known to accompany acute myocardial ischemia, but its role in the pathogenesis of ischemic heart disease is unclear. In this study, we aimed to determine how ceramides accumulate in the ischemic heart and to determine if cardiac function following ischemia can be improved by reducing ceramide accumulation. To investigate the association between ceramide accumulation and heart function, we analyzed myocardial left ventricle biopsies from subjects with chronic ischemia and found that ceramide levels were higher in biopsies from subjects with reduced heart function. Ceramides are produced by either de novo synthesis or hydrolysis of sphingomyelin catalyzed by acid and/or neutral sphingomyelinase. We used cultured HL-1 cardiomyocytes to investigate these pathways and showed that acid sphingomyelinase activity rather than neutral sphingomyelinase activity or de novo sphingolipid synthesis was important for hypoxia-induced ceramide accumulation. We also used mice with a partial deficiency in acid sphingomyelinase (Smpd1(+/-) mice) to investigate if limiting ceramide accumulation under ischemic conditions would have a beneficial effect on heart function and survival. Although we showed that cardiac ceramide accumulation was reduced in Smpd1(+/-) mice 24 h after an induced myocardial infarction, this reduction was not accompanied by an improvement in heart function or survival. Our findings show that accumulation of cardiac ceramides in the post-ischemic heart is mediated by acid sphingomyelinase. However, targeting ceramide accumulation in the ischemic heart may not be a beneficial treatment strategy.
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3.
  • Lundqvist, Annika, 1969, et al. (författare)
  • The Arachidonate 15-Lipoxygenase Enzyme Product 15-HETE Is Present in Heart Tissue from Patients with Ischemic Heart Disease and Enhances Clot Formation
  • 2016
  • Ingår i: Plos One. - : Public Library of Science (PLoS). - 1932-6203. ; 11:8
  • Tidskriftsartikel (refereegranskat)abstract
    • Ischemic heart disease is a major cause of death and morbidity and the search for novel therapeutic targets is still required. We have previously shown that the enzyme arachidonate 15 lipoxygenase (ALOX15), which catalyzes the conversion of arachidonic acid to 15-hydroxy eicosatetraenoic acid (15-HETE), is highly expressed in ischemic heart tissue, but its role in the pathogenesis of ischemic heart disease is unclear. Here we showed that expression of ALOX15, but not ALOX12 or ALOX15B, was increased in ischemic versus non-ischemic human heart biopsy samples. A similar ALOX expression pattern was found in hypoxic human cardiomyocytes and cardiac endothelial cells. We also showed that levels of 15-HETE were significantly higher in ischemic versus non-ischemic human heart biopsy samples and showed a tendency to increase in serum from the patients with ischemic heart disease. Moreover, hypoxia increased the production of 15-HETE levels from human cardiomyocytes and cardiac endothelial cells. The hypoxia-induced increase in 15-HETE levels from human cardiomyocytes was inhibited by the ALOX15 inhibitor baicalein. Finally, by using intrinsic rotational thromboelastometry, we showed that human whole blood clotted faster in the presence of 15-HETE. In summary, we propose that increased ALOX15 expression in heart tissue under ischemic conditions may lead to increased production of 15-HETE, potentially contributing to thrombosis.
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4.
  • Rotter Sopasakis, Victoria, 1972, et al. (författare)
  • Toll-like receptor-mediated inflammation markers are strongly induced in heart tissue in patients with cardiac disease under both ischemic and non-ischemic conditions.
  • 2019
  • Ingår i: International journal of cardiology. - : Elsevier BV. - 1874-1754 .- 0167-5273. ; 293, s. 238-247
  • Tidskriftsartikel (refereegranskat)abstract
    • A sustained low grade inflammatory state is a recognized feature of various diseases, including cardiovascular disease. This state of chronic inflammation involves activation of Toll-like receptor (TLR) signaling. However, little is known regarding the genetic profile of TLR components in cardiac tissue from patients with cardiac disease.In this study we investigated the genetic profile of 84 TLR markers in a unique set of cardiac tissue from patients that had undergone either coronary artery bypass grafting (CABG) or aortic valve replacement (AVR). In addition, we compared the gene data from the cardiac tissue with the same gene profile in blood as well as circulating cytokines to elucidate possible targets in blood that could be used to estimate the inflammatory state of the heart in cardiac disease.We found a marked upregulation of TLR-induced inflammation in cardiac tissue from both patient groups compared to healthy controls. The inflammation appeared to be primarily mediated through TLR1, 3, 7, 8 and 10, resulting in a marked induction of mediators of the innate immune response. Furthermore, the gene expression data in combination with unbiased multivariate analysis suggested a difference in inflammatory response in ischemic cardiac tissue compared to non-ischemic cardiac tissue. Serum levels of IL-13 were significantly elevated in both CABG and AVR patients compared to controls, whereas other cytokines did not appear to coincide with cardiac TLR-induced inflammation.We propose that cardiac disease in humans may be mediated by local cardiac TLR signaling under both ischemic and non-ischemic conditions.
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5.
  • Sandstedt, Joakim, et al. (författare)
  • Human cardiac fibroblasts isolated from patients with severe heart failure are immune-competent cells mediating an inflammatory response.
  • 2019
  • Ingår i: Cytokine. - : Elsevier BV. - 1096-0023 .- 1043-4666. ; 113, s. 319-325
  • Tidskriftsartikel (refereegranskat)abstract
    • This study was aimed to elucidate the immunoregulatory properties of human cardiac fibroblasts cultured under pro-inflammatory and hypoxic conditions. Human heart tissue for isolating cardiac cells is generally hard to obtain, particularly from all four chambers of the same heart. Since different parts of the heart have different functions and therefore may have different immunoregulatory properties, ability to analyse cells from all chambers allows for a unique and comprehensive investigation. Cells were isolated from all four chambers of the heart from patients undergoing cardiac transplantation surgery due to severe chronic heart failure (CHF) (n = 6). Cells isolated from one donor heart, were used for comparison with the experimental group. Primary cultured human cardiac fibroblasts were treated with Lipopolysaccharide (LPS) to induce an inflammatory response. Cells were also subjected to hypoxia. To determine immunoregulatory properties of the cells, cytokine and chemokine profiles were determined using multiplex ELISA. RESULTS: On average, the fibroblasts population constituted approximately 90% of the expanded non-myocytes. Levels of cytokines and chemokines were markedly increased in human cardiac fibroblasts cultured under inflammatory conditions, with a similar response in fibroblasts from all compartments of the heart. Unexpectedly, hypoxia did not further augment cytokine and chemokine secretion. In conclusion, human cardiac fibroblasts are a robust source of pro-inflammatory mediators in the failing heart, independent of hypoxia, and might play a critical role in inflammation associated with the pathogenesis of CHF.
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  • Resultat 1-5 av 5

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