Abstract

Patients with rheumatoid arthritis (RA) have a higher risk for atherosclerosis. There is no clinical information about scavenger receptor CD36 and the development of subclinical atherosclerosis in patients with RA. The aim of this study was to evaluate the association between membrane expression of CD36 in peripheral blood mononuclear cells (PBMC) and carotid intima-media thickness (cIMT) in patients with RA. Methods. We included 67 patients with RA from the Rheumatology Department of Hospital Civil “Dr. Juan I. Menchaca,” Guadalajara, Jalisco, Mexico. We evaluated the cIMT, considering subclinical atherosclerosis when >0.6 mm. Since our main objective was to associate the membrane expression of CD36 with subclinical atherosclerosis, other molecules related with cardiovascular risk such as ox-LDL, IL-6, and TNFα were tested. Results. We found low CD36 membrane expression in PBMC from RA patients with subclinical atherosclerosis (P < 0.001). CD36 mean fluorescence intensity had negative correlations with cIMT (r = −0.578, P < 0.001), ox-LDL (r = −0.427, P = 0.05), TNFα (r = −0.729, P < 0.001), and IL-6 (r = −0.822, P < 0.001). Conclusion. RA patients with subclinical atherosclerosis showed low membrane expression of CD36 in PBMC and increased serum proinflammatory cytokines. Further studies are needed to clarify the regulation of CD36 in RA.

Highlights

  • Rheumatoid arthritis (RA) is a chronic autoimmune disease with systemic complications and early cardiovascular death [1]

  • Since our main objective was to associate the membrane expression of CD36 with subclinical atherosclerosis, other molecules related with cardiovascular risk such as oxidized low density lipoproteins (ox-LDL), IL-6, and TNFα were tested

  • We showed that rheumatoid arthritis (RA) patients with subclinical atherosclerosis showed low membrane expression of CD36 in peripheral blood mononuclear cells (PBMC) and increased serum proinflammatory cytokines (Table 1)

Read more

Summary

Introduction

Rheumatoid arthritis (RA) is a chronic autoimmune disease with systemic complications and early cardiovascular death [1]. Atherosclerosis and inflammation in RA share several mechanisms in their pathogenesis including proinflammatory cytokine expression, infectious agents, dyslipidemia, and autoantibodies [2,3,4,5,6,7,8]. Blood monocytes are recruited into the intima and subintima layers of blood vessels; were they internalize oxidized low density lipoproteins (ox-LDL) through SR (CD36). CD36 has a critical role in the atherosclerotic plaque development [11,12,13,14]. Their role in cardiovascular complications of RA has not been studied

Objectives
Methods
Results
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call