8 results on '"Stemme V"'
Search Results
2. Expression of Cyclo-oxygenase-2 in Human Atherosclerotic Carotid Arteries
- Author
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Stemme, V, primary, Swedenborg, J, additional, Claesson, H -E, additional, and Hansson, GK, additional
- Published
- 2000
- Full Text
- View/download PDF
3. CXCL16 is an interferon-γ regulated chemokine and scavenger receptor expressed in atherosclerotic lesions
- Author
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Wuttge, D.M., Zhou, X., Sheikine, Y., Stemme, V., Hedin, U., Stemme, S., Hansson, G.K., and Sirsjo, A.
- Subjects
Heart diseases -- Research ,Health ,Research - Abstract
D.M. Wuttge (*) X. Zhou (*) U. Hedin (1) Background: A growing body of evidence implies that atherosclerosis is an inflammatory disease. Activated macrophages and T cells guided by adhesion [...]
- Published
- 2002
4. Quantitative analysis of specific mRNA species in minute cell samples by RT-PCR and flow cytometry
- Author
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Stemme, V., Rymo, L., Risberg, B., and Stemme, S.
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- 2001
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- View/download PDF
5. Regulation and splicing of scavenger receptor class B type I in human macrophages and atherosclerotic plaques
- Author
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Fagerberg Björn, Thelle Dag S, Mattsson-Hulten Lillemor, Stemme Veronika, Ohlsson Bertil G, Hägg Daniel A, Snäckestrand Magnus SC, Englund Mikael CO, Svensson Per-Arne, Wiklund Olov, Carlsson Lena MS, and Carlsson Björn
- Subjects
Diseases of the circulatory (Cardiovascular) system ,RC666-701 - Abstract
Abstract Background The protective role of high-density lipoprotein (HDL) in the cardiovascular system is related to its role in the reverse transport of cholesterol from the arterial wall to the liver for subsequent excretion via the bile. Scavenger receptor class B type I (SR-BI) binds HDL and mediates selective uptake of cholesterol ester and cellular efflux of cholesterol to HDL. The role of SR-BI in atherosclerosis has been well established in murine models but it remains unclear whether SR-BI plays an equally important role in atherosclerosis in humans. The aim of this study was to investigate the expression of SR-BI and its isoforms in human macrophages and atherosclerotic plaques. Methods The effect of hypoxia and minimally modified low-density lipoprotein (mmLDL), two proatherogenic stimuli, on SR-BI expression was studied in human monocyte-derived macrophages from healthy subjects using real-time PCR. In addition, SR-BI expression was determined in macrophages obtained from subjects with atherosclerosis (n = 15) and healthy controls (n = 15). Expression of SR-BI isoforms was characterized in human atherosclerotic plaques and macrophages using RT-PCR and DNA sequencing. Results SR-BI expression was decreased in macrophages after hypoxia (p < 0.005). In contrast, SR-BI expression was increased by exposure to mmLDL (p < 0.05). There was no difference in SR-BI expression in macrophages from patients with atherosclerosis compared to controls. In both groups, SR-BI expression was increased by exposure to mmLDL (p < 0.05). Transcripts corresponding to SR-BI and SR-BII were detected in macrophages. In addition, a third isoform, referred to as SR-BIII, was discovered. All three isoforms were also expressed in human atherosclerotic plaque. Compared to the other isoforms, the novel SR-BIII isoform was predicted to have a unique intracellular C-terminal domain containing 53 amino acids. Conclusion We conclude that SR-BI is regulated by proatherogenic stimuli in humans. However, we found no differences between subjects with atherosclerosis and healthy controls. This indicates that altered SR-BI expression is not a common cause of atherosclerosis. In addition, we identified SR-BIII as a novel isoform expressed in human macrophages and in human atherosclerotic plaques.
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- 2005
- Full Text
- View/download PDF
6. Regulation and splicing of scavenger receptor class B type I in human macrophages and atherosclerotic plaques.
- Author
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Svensson PA, Englund MC, Snäckestrand MS, Hägg DA, Ohlsson BG, Stemme V, Mattsson-Hulten L, Thelle DS, Fagerberg B, Wiklund O, Carlsson LM, and Carlsson B
- Subjects
- Adult, Alternative Splicing, Amino Acid Motifs, Amino Acid Sequence, Atherosclerosis etiology, Atherosclerosis metabolism, Base Sequence, Cell Hypoxia, Cells, Cultured, Female, Gene Expression Regulation drug effects, Humans, Lipoproteins, LDL pharmacology, Lysosomal Membrane Proteins chemistry, Lysosomal Membrane Proteins genetics, Lysosomal Membrane Proteins metabolism, Macrophages drug effects, Male, Molecular Sequence Data, Protein Isoforms, RNA, Messenger metabolism, Receptors, Scavenger, Scavenger Receptors, Class B chemistry, Scavenger Receptors, Class B genetics, Sialoglycoproteins chemistry, Sialoglycoproteins genetics, Sialoglycoproteins metabolism, src Homology Domains, Macrophages metabolism, Scavenger Receptors, Class B metabolism
- Abstract
Background: The protective role of high-density lipoprotein (HDL) in the cardiovascular system is related to its role in the reverse transport of cholesterol from the arterial wall to the liver for subsequent excretion via the bile. Scavenger receptor class B type I (SR-BI) binds HDL and mediates selective uptake of cholesterol ester and cellular efflux of cholesterol to HDL. The role of SR-BI in atherosclerosis has been well established in murine models but it remains unclear whether SR-BI plays an equally important role in atherosclerosis in humans. The aim of this study was to investigate the expression of SR-BI and its isoforms in human macrophages and atherosclerotic plaques., Methods: The effect of hypoxia and minimally modified low-density lipoprotein (mmLDL), two proatherogenic stimuli, on SR-BI expression was studied in human monocyte-derived macrophages from healthy subjects using real-time PCR. In addition, SR-BI expression was determined in macrophages obtained from subjects with atherosclerosis (n = 15) and healthy controls (n = 15). Expression of SR-BI isoforms was characterized in human atherosclerotic plaques and macrophages using RT-PCR and DNA sequencing., Results: SR-BI expression was decreased in macrophages after hypoxia (p < 0.005). In contrast, SR-BI expression was increased by exposure to mmLDL (p < 0.05). There was no difference in SR-BI expression in macrophages from patients with atherosclerosis compared to controls. In both groups, SR-BI expression was increased by exposure to mmLDL (p < 0.05). Transcripts corresponding to SR-BI and SR-BII were detected in macrophages. In addition, a third isoform, referred to as SR-BIII, was discovered. All three isoforms were also expressed in human atherosclerotic plaque. Compared to the other isoforms, the novel SR-BIII isoform was predicted to have a unique intracellular C-terminal domain containing 53 amino acids., Conclusion: We conclude that SR-BI is regulated by proatherogenic stimuli in humans. However, we found no differences between subjects with atherosclerosis and healthy controls. This indicates that altered SR-BI expression is not a common cause of atherosclerosis. In addition, we identified SR-BIII as a novel isoform expressed in human macrophages and in human atherosclerotic plaques.
- Published
- 2005
- Full Text
- View/download PDF
7. CXCL16/SR-PSOX is an interferon-gamma-regulated chemokine and scavenger receptor expressed in atherosclerotic lesions.
- Author
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Wuttge DM, Zhou X, Sheikine Y, Wågsäter D, Stemme V, Hedin U, Stemme S, Hansson GK, and Sirsjö A
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- Animals, Apolipoproteins E deficiency, Apolipoproteins E genetics, Arteriosclerosis genetics, Arteriosclerosis metabolism, Carotid Artery Diseases immunology, Cell Line, Chemokine CXCL16, Chemokine CXCL6, Chemokines, CXC biosynthesis, Chemokines, CXC genetics, Chemotaxis, Leukocyte drug effects, Cholesterol metabolism, Female, Humans, Interferon-gamma pharmacology, Lipoproteins, LDL metabolism, Membrane Proteins biosynthesis, Membrane Proteins genetics, Mice, Mice, Inbred C57BL, Mice, Knockout, Models, Animal, Monocytes drug effects, Monocytes metabolism, RNA, Messenger biosynthesis, Receptors, CXCR, Receptors, CXCR6, Receptors, Chemokine biosynthesis, Receptors, Chemokine genetics, Receptors, Cytokine biosynthesis, Receptors, Cytokine genetics, Receptors, G-Protein-Coupled biosynthesis, Receptors, G-Protein-Coupled genetics, Receptors, Immunologic biosynthesis, Receptors, Immunologic genetics, Receptors, Scavenger, Receptors, Virus biosynthesis, Receptors, Virus genetics, T-Lymphocytes drug effects, Up-Regulation drug effects, Carotid Artery Diseases metabolism, Chemokines, CXC physiology, Foam Cells metabolism, Interferon-gamma physiology, Membrane Proteins physiology, Receptors, Immunologic physiology
- Abstract
Objective: Atherosclerosis is an inflammatory disease. Several chemokines are important for monocyte/macrophage and T-cell recruitment to the lesion. CXCL16 is a recently discovered chemokine that is expressed in soluble and transmembrane forms, ligates CXCR6 chemokine receptor, and guides migration of activated Th1 and Tc1 cells. It is identical to scavenger receptor SR-PSOX, which mediates uptake of oxidized low-density lipoprotein. We investigated whether CXCL16 expression is controlled by interferon-gamma (IFN-gamma)-cytokine abundant in atherosclerotic lesions., Methods and Results: CXCL16 and CXCR6 expression was identified by polymerase chain reaction and histochemistry in atherosclerotic lesions from humans and apolipoprotein-E-deficient mice. In vitro IFN-gamma induced CXCL16 in human monocytic THP-1 cells and primary human monocytes, which led to increased uptake of oxidized low-density lipoprotein in THP-1 cells, which could be blocked by peptide antibodies against CXCL16. In vivo IFN-gamma induced CXCL16 expression in murine atherosclerotic lesions., Conclusions: We demonstrate a novel role of IFN-gamma in foam cell formation through upregulation of CXCL16/SR-PSOX. CXCR6 expression in the plaque confirms the presence of cells able to respond to CXCL16. Therefore, this chemokine/scavenger receptor could serve as a molecular link between lipid metabolism and immune activity in the atherosclerotic lesion.
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- 2004
- Full Text
- View/download PDF
8. Regional variation in plasminogen activator inhibitor-1 expression in adipose tissue from obese individuals.
- Author
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Eriksson P, Van Harmelen V, Hoffstedt J, Lundquist P, Vidal H, Stemme V, Hamsten A, Arner P, and Reynisdottir S
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- Adipose Tissue pathology, Adult, Body Mass Index, Cell Size, Disease Susceptibility, Female, Humans, Male, Middle Aged, Obesity pathology, Organ Specificity, Plasminogen Activator Inhibitor 1 genetics, Plasminogen Activator Inhibitor 1 metabolism, RNA, Messenger biosynthesis, Skin pathology, Tumor Necrosis Factor-alpha metabolism, Viscera pathology, Adipose Tissue metabolism, Gene Expression Regulation, Obesity metabolism, Plasminogen Activator Inhibitor 1 biosynthesis
- Abstract
High plasma plasminogen activator inhibitor-1 (PAI-1) activity is a frequent finding in obesity and adipose tissue has recently been suggested to be a source of circulating PAI-1 in humans. In the present study, differences in adipose tissue gene expression and protein secretion rate of PAI-1 between subcutaneous and visceral adipose tissue was analysed in specimens obtained from 22 obese individuals. The secretion rate of PAI-1 was two-fold higher in subcutaneous adipose tissue than in visceral adipose tissue (292 +/- 50 vs 138 +/- 24 ng PAI-1/10(7) cells, P <0.05). In accordance with the secretion data, subcutaneous adipose tissue contained about three-fold higher levels of PAI-1 mRNA than visceral adipose tissue (2.43 +/- 0.37 vs 0.81 +/- 0.12 attomole PAI-1 mRNA/microg total RNA, P <0.00 ). PAI-1 secretion from subcutaneous but not from visceral adipose tissue correlated significantly with cell size (r = 0.43, P<0.05). In summary, subcutaneous adipose tissue secreted greater amounts of PAI-1 and had a higher PAI-1 gene expression than visceral adipose tissue from the same obese individuals. Bearing in mind that subcutaneous adipose tissue is the largest fat depot these finding may be important for the coagulation abnormalities associated with obesity.
- Published
- 2000
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