| 1. |
- Abedpour Dehkordi, Adel, et al.
(författare)
-
Interleukin-6 reduces paraoxonase-1 activity in a dose-dependent manner : evidence for a potential novel lipoprotein-based modulatory mechanism
- 2016
-
Ingår i: Atherosclerosis. - : Elsevier. - 0021-9150 .- 1879-1484. ; 252, s. E113-E114
-
Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- Objectives: The anti-oxidant/anti-inflammatory nature of HDL is mainly associated with paraoxonase-1 (PON1). Previous studies have revealed an inverse correlation between Interleukin-6 (IL-6) and PON1 expression. The current study investigates the effect of IL-6 on serum PON1 activity in vitro, given the potential structural capability of PON1 to host multiple ligands. Methods: PON1 activity was measured spectrophotometrically (234 nm) using paraoxon substrate in the presence of concentrations of IL-6 than control samples. A sequence alignment using the FASTA sequence was manually conducted to identify possible homologies between PON1 and the IL-6-binding protein. Statistical analysis was conducted using GraphPad Prism v5.0. Results: PON1 enzyme activity decreased by 15%, 26% (P<0.05) and 55% (P<0.001) in the presence of 4, 10 and 20 pg/ml of IL-6, respectively. in comparison with the controls. Student t. test was used as statistical method (p<0.05: statistically significant). There are potential homologies between PON1 active sites and know IL-6-binding residues. Conclusions: This study shows that IL-6 directly reduce the PON1 activity in a dose-dependent manner. This observation supports some studies indicating inverse correlation between PON1 and IL-6. However, as opposed to the gene-mediated approach, this study suggest that IL-6 may act directly through specific binding to PON1 (biochemical modulation). X ray crystallography can further scrutinize the present finding.
|
|
| 2. |
|
|
| 3. |
|
|
| 4. |
|
|
| 5. |
|
|
| 6. |
- Antoniewicz, Lukasz, et al.
(författare)
-
Electronic cigarettes increase endothelial progenitor cells in the blood of healthy volunteers
- 2016
-
Ingår i: Atherosclerosis. - : Elsevier BV. - 0021-9150 .- 1879-1484. ; 255, s. 179-185
-
Tidskriftsartikel (refereegranskat)abstract
- Background and aims: The use of electronic cigarettes is increasing dramatically on a global scale and its effects on human health remain uncertain. In the present study, we measured endothelial progenitor cells (EPCs) and microvesicles (MVs) in healthy young volunteers following short-term exposure to inhalation of e-cigarette vapor (ECV) to determine vascular changes.Methods: Sixteen healthy seldom smokers were randomized into two groups either exposed or not exposed to 10 puffs of ECV for 10 min, in a crossover design. Blood samples were obtained at baseline and 1, 4 and 24 h following exposure. EPCs (CD34 + CD309) and MVs were analyzed by flow cytometry. MVs were phenotyped according to origin (platelet (CD41), endothelial (CD144), leukocytes (CD45), monocytes (CD14)) and nuclear content (SYTO 13 dye). In addition, expression of inflammation markers such P-selectin (CD62P), E-selectin (CD62E), CD40-ligand (CD154) and HMGB1 was investigated. Fractional exhaled nitric oxide (FeNO) was also measured at baseline and after 24 h.Results: EPC levels in blood were significantly increased 1 h following exposure to ECV and returned to baseline values after 24 h. Only E-selectin positive MVs (endothelial origin) were slightly elevated (p < 0.038). FeNO was unaffected by exposure to ECV. Conclusions: In healthy volunteers, ten puffs of e-cigarette vapor inhalation caused an increase in EPCs. This increase was of the same magnitude as following smoking of one traditional cigarette, as we previously demonstrated. Taken together, these results may represent signs of possible vascular changes after short e-cigarette inhalation. Further studies analyzing potential cardiovascular health effects are critical as the e-cigarette market continues to burgeon.
|
|
| 7. |
|
|
| 8. |
|
|
| 9. |
|
|
| 10. |
- Carlsson, Axel C, et al.
(författare)
-
Levels of soluble tumor necrosis factor receptor 1 and 2, gender, and risk of myocardial infarction in Northern Sweden
- 2018
-
Ingår i: Atherosclerosis. - : Elsevier BV. - 0021-9150 .- 1879-1484. ; 272, s. 41-46
-
Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND AND AIMS: Soluble receptors for tumor necrosis factor alpha (sTNFR1 and sTNFR2) have been associated with cardiovascular diseases, and some evidence points towards a difference in associated risk between men and women. We aimed to study the association between sTNFR1 and sTNFR2 and incident myocardial infarctions (MI) and to explore the influence of established cardiovascular risk factors in men and women.METHODS: We conducted a nested case control study in three large Swedish cohorts, including 533 myocardial infarction cases, and 1003 age-, sex- and cohort-matched controls. Odds ratios (OR) with 95% confidence intervals (CI) were calculated.RESULTS: An association between circulating sTNFR1 and sTNFR2 and an increased risk for MI was found when comparing cases and controls. The odds ratios were significant after adjustment for established cardiovascular risk factors and C-reactive protein in women (OR 1.44, 95% CI 1.08-1.93 for TNFR1, and 1.61, 95% CI 1.11-2.34 for TNFR2), but was abolished in men. Women with a combination of elevated CRP and values in the upper quartile of TNFR1 or TNFR2 had a 5-fold higher risk of myocardial infarction versus those with normal CRP and values in the lower three quartiles of TNFR1 or TNFR2.CONCLUSIONS: As the risk estimates for TNFR1 and TNFR2 were higher and remained significant after adjustments for established cardiovascular risk factors in women but not in men, a potential role for TNFR1 and TNFR2 in identifying women with a higher MI risk is possible. The future clinical role of TNFR1 and TNFR2 in combination with CRP to identify high risk patients for coronary heart disease has yet to be determined.
|
|
