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Biosensors (Basel). 2019 Feb 27;9(1). pii: E32. doi: 10.3390/bios9010032.

Plasma from Patients with Rheumatoid Arthritis Reduces Nitric Oxide Synthesis and Induces Reactive Oxygen Species in A Cell-Based Biosensor.

Author information

1
Department of Clinical Biochemistry and Immunology, Faculty of Pharmacy, Universidad de Concepción, Victor Lamas 1290, Concepcion 4030000, Chile. herbert.herlitz@uss.cl.
2
Facultad de Ciencias de la Salud, Universidad San Sebastián, Lientur 1457, Concepcion 4030000, Chile. herbert.herlitz@uss.cl.
3
Department of Clinical Biochemistry and Immunology, Faculty of Pharmacy, Universidad de Concepción, Victor Lamas 1290, Concepcion 4030000, Chile. camilavejar@udec.cl.
4
Clinical and Genetic Laboratory PreveGen, Chacabuco 556, Concepcion 4030000, Chile. camilavejar@udec.cl.
5
Department of Clinical Biochemistry and Immunology, Faculty of Pharmacy, Universidad de Concepción, Victor Lamas 1290, Concepcion 4030000, Chile. daniale.floresf@gmail.com.
6
Department of Clinical Biochemistry and Immunology, Faculty of Pharmacy, Universidad de Concepción, Victor Lamas 1290, Concepcion 4030000, Chile. paojara@udec.cl.
7
Department of Clinical Biochemistry and Immunology, Faculty of Pharmacy, Universidad de Concepción, Victor Lamas 1290, Concepcion 4030000, Chile. pbustos@udec.cl.
8
Department of Rheumatology, Regional Clinical Hospital Dr. Guillermo Grant Benavente, San Martin 1436, Concepcion 4030000, Chile. ircastro@udec.cl.
9
Department of Internal Medicine. Faculty of Medicine, Universidad de Concepción, Victor Lamas 1290, Concepcion 4030000, Chile. ircastro@udec.cl.
10
Department of Clinical Biochemistry and Immunology, Faculty of Pharmacy, Universidad de Concepción, Victor Lamas 1290, Concepcion 4030000, Chile. epoblete1@uc.cl.
11
Department of Statistics, Faculty of Physical Sciences and Mathematics, Universidad de Concepción, Victor Lamas 1290, Concepcion 4030000, Chile. ksaez@udec.cl.
12
Central Clinical Laboratory, Regional Clinical Hospital Dr. Guillermo Grant Benavente, San Martin 1436, Concepcion 4030000, Chile. mopazo@ssconcepcion.cl.
13
Department of Internal Medicine. Faculty of Medicine, Universidad de Concepción, Victor Lamas 1290, Concepcion 4030000, Chile. jgncardio@gmail.com.
14
Department of Clinical Biochemistry and Immunology, Faculty of Pharmacy, Universidad de Concepción, Victor Lamas 1290, Concepcion 4030000, Chile. caguayo@udec.cl.
15
Department of Clinical Biochemistry and Immunology, Faculty of Pharmacy, Universidad de Concepción, Victor Lamas 1290, Concepcion 4030000, Chile. enovalamperti@gmail.com.
16
Clinical and Genetic Laboratory PreveGen, Chacabuco 556, Concepcion 4030000, Chile. enovalamperti@gmail.com.
17
Department of Clinical Biochemistry and Immunology, Faculty of Pharmacy, Universidad de Concepción, Victor Lamas 1290, Concepcion 4030000, Chile. llampert@udec.cl.
18
Clinical and Genetic Laboratory PreveGen, Chacabuco 556, Concepcion 4030000, Chile. llampert@udec.cl.

Abstract

Rheumatoid arthritis (RA) has been associated with a higher risk of developing cardiovascular (CV) diseases. It has been proposed that systemic inflammation plays a key role in premature atherosclerosis development, and is therefore crucial to determine whether systemic components from RA patients promotes endothelial cell-oxidative stress by affecting reactive oxygen species (ROS) and nitric-oxide (NO) production. The aim of this study was to evaluate whether plasma from RA patients impair NO synthesis and ROS production by using the cell-line ECV-304 as a biosensor. NO synthesis and ROS production were measured in cells incubated with plasma from 73 RA patients and 52 healthy volunteers by fluorimetry. In addition, traditional CV risk factors, inflammatory molecules and disease activity parameters were measured. Cells incubated with plasma from RA patients exhibited reduced NO synthesis and increased ROS production compared to healthy volunteers. Furthermore, the imbalance between NO synthesis and ROS generation in RA patients was not associated with traditional CV risk factors. Our data suggest that ECV-304 cells can be used as a biosensor of systemic inflammation-induced endothelial cell-oxidative stress. We propose that both NO and ROS production are potential biomarkers aimed at improving the current assessment of CV risk in RA.

KEYWORDS:

cardiovascular (CV) diseases; endothelial cell-oxidative stress; rheumatoid arthritis

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