Objectives: Circulating proangiogenic haematopoietic cells (PHCs), including CD34+ cells, play an important role in endothelial homeostasis. Among PHCs, CD34+ cells are the largest cell population, thus, much of the regenerative/reparative potential of PHCs may be attributed to CD34+ cells. Our aim was to determine the association between inflammation and CD34+ cell number, intracellular levels of reactive oxygen species (ROS) and expression of Toll-like receptor 3 (TLR3) and interleukin 1β (IL-1β), arterial stiffness (AS) indices, and carotid intima-media thickness (cIMT) in patients affected by rheumatoid arthritis (RA).

Methods: CD34+ cells were isolated from 24 RA patients and 26 matched controls. ROS levels, TLR3 and IL-1β expression were measured. C-reactive protein (CRP), fibrinogen, AS, and cIMT were also evaluated.

Results: CD34+ count was lower in RA patients as compared to controls. In CD34+ cells from RA patients, ROS, TLR3 and IL-1β expressions were increased compared to controls. In RA patients, we found higher CRP and fibrinogen levels, and higher values of Pulse Wave Velocity (PWV) and Augmentation Index (AIx), both AS indices, and of cIMT. CD34+ cell numbers were inversely correlated with CRP, TLR3, IL-1β, ROS, and AS indices. TLR3 levels were related to CRP, IL-1β, fibrinogen and ROS. IL-1β levels were correlated with expression of CRP, ROS, and PWV.

Conclusions: Inflammatory status in RA is associated with an increased expression of TLR3 and of IL-1β in CD34+ cells, which appear to affect cell number. These new findings suggest a perspective on accelerated atherosclerosis and vascular damage in RA.

Download full-text PDF

Source

Publication Analysis

Top Keywords

cd34+ cells
28
tlr3 il-1β
16
cd34+
10
toll-like receptor
8
interleukin 1β
8
cells
8
cells patients
8
patients rheumatoid
8
rheumatoid arthritis
8
association inflammation
8

Similar Publications

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!