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The red blood cell ...
The red blood cell as a mediator of endothelial dysfunction in patients with familial hypercholesterolemia and dyslipidemia
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- Mahdi, A. (författare)
- Karolinska Institutet
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- Wodaje, T. (författare)
- Karolinska Institutet
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- Kovamees, O. (författare)
- Karolinska Institutet
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- Tengbom, J. (författare)
- Karolinska Institutet
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- Zhao, A. (författare)
- Karolinska Institutet
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Jiao, T. (författare)
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- Henricsson, Marcus, 1975 (författare)
- Gothenburg University,Göteborgs universitet,Institutionen för medicin, avdelningen för molekylär och klinisk medicin,Wallenberglaboratoriet,Institute of Medicine, Department of Molecular and Clinical Medicine,Wallenberg Laboratory
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Yang, J. N. (författare)
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- Zhou, Z. C. (författare)
- Karolinska Institutet
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Nieminen, A. I. (författare)
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- Levin, Malin, 1973 (författare)
- Gothenburg University,Göteborgs universitet,Wallenberglaboratoriet,Institutionen för medicin, avdelningen för molekylär och klinisk medicin,Wallenberg Laboratory,Institute of Medicine, Department of Molecular and Clinical Medicine
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- Collado, A. (författare)
- Karolinska Institutet
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- Brinck, J. (författare)
- Karolinska Institutet
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- Pernow, J. (författare)
- Karolinska Institutet
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(creator_code:org_t)
- 2022-11-02
- 2023
- Engelska.
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Ingår i: Journal of Internal Medicine. - : Wiley. - 0954-6820 .- 1365-2796. ; 293:2, s. 228-245
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Abstract
Ämnesord
Stäng
- Background Patients with familial hypercholesterolemia (FH) display high levels of low-density lipoprotein cholesterol (LDL-c), endothelial dysfunction, and increased risk of premature atherosclerosis. We have previously shown that red blood cells (RBCs) from patients with type 2 diabetes induce endothelial dysfunction through increased arginase 1 and reactive oxygen species (ROS). Objective To test the hypothesis that RBCs from patients with FH (FH-RBCs) and elevated LDL-c induce endothelial dysfunction. Methods and results FH-RBCs and LDL-c >5.0 mM induced endothelial dysfunction following 18-h incubation with isolated aortic rings from healthy rats compared to FH-RBCs and LDL-c <2.5 mM or RBCs from healthy subjects (H-RBCs). Inhibition of vascular but not RBC arginase attenuated the degree of endothelial dysfunction induced by FH-RBCs and LDL-c >5.0 mM. Furthermore, arginase 1 but not arginase 2 was elevated in the vasculature of aortic segments after incubation with FH-RBCs and LDL-c >5.0 mM. A superoxide scavenger, present throughout the 18-h incubation, attenuated the degree of endothelial dysfunction induced by FH-RBCs and LDL-c >5.0 mM. ROS production was elevated in these RBCs in comparison with H-RBCs. Scavenging of vascular ROS through various antioxidants also attenuated the degree of endothelial dysfunction induced by FH-RBCs and LDL-c >5.0 mM. This was corroborated by an increase in the lipid peroxidation product 4-hydroxynonenal. Lipidomic analysis of RBC lysates did not reveal any significant changes across the groups. Conclusion FH-RBCs induce endothelial dysfunction dependent on LDL-c levels via arginase 1 and ROS-dependent mechanisms.
Ämnesord
- MEDICIN OCH HÄLSOVETENSKAP -- Klinisk medicin -- Kardiologi (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Clinical Medicine -- Cardiac and Cardiovascular Systems (hsv//eng)
Nyckelord
- arginase
- endothelial dysfunction
- familial hypercholesterolemia
- low-density lipoprotein
- reactive oxygen species
- red blood cell
- nitric-oxide synthase
- erythrocytes
- cholesterol
- deformability
- export
- General & Internal Medicine
Publikations- och innehållstyp
- ref (ämneskategori)
- art (ämneskategori)
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Till lärosätets databas
- Av författaren/redakt...
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Mahdi, A.
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Wodaje, T.
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Kovamees, O.
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Tengbom, J.
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Zhao, A.
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Jiao, T.
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visa fler...
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Henricsson, Marc ...
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Yang, J. N.
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Zhou, Z. C.
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Nieminen, A. I.
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Levin, Malin, 19 ...
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Collado, A.
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Brinck, J.
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Pernow, J.
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visa färre...
- Om ämnet
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- MEDICIN OCH HÄLSOVETENSKAP
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MEDICIN OCH HÄLS ...
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och Klinisk medicin
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och Kardiologi
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Journal of Inter ...
- Av lärosätet
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Göteborgs universitet
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Karolinska Institutet