Platelet Activation Markers and Soluble Adhesion Molecules in Patients with Systemic Lupus Erythematosus

Abstract

We assessed the role of platelet activation markers (PMPs, Annexin V and CD62P on activated platelets), cytokines (IL-1 beta, IL-4, IL-6, IFN- gamma, GM-CSF, and TNF alpha ), and soluble factors (sIL-2R, TM, sHLA-1, beta(2) -m, sVCAM-1, sPECAM-1, sP-selectin and sE-selectin) in vascular damage related to SLE. There were differences in the levels of PMPs and platelet activation markers between the SLE patients and controls (PMPs: 493+/-82 vs. 328+/-36, p<0.05; plt-CD62P; 8.5%+/-1.2 % vs. 4.6%+/-0.7 %, p<0.05; plt-Annexin V: 11.3%+/-2.1 % vs. 4.9%+/-0.6 %, p<0.01). There were no differences in the levels of IFN- gamma between the groups. However, the levels of IL-1 beta, IL-4, IL-6, GM-CSF, TNF alpha, and soluble factors were higher in the SLE patients than in the controls. The levels of IL-4, IL-6, beta2 -m, sIL-2R, sVCAM-1, sP-selectin, and sE-selectin in SLE patients with elevated sTM levels were higher than those in the SLE patients without elevated sTM levels. On the other hand, elevations of sIL-2R, sVCAM-1, and sP-selectin were not found in patients with Behçet disease or rheumatoid arthritis. The levels of platelet CD62P, platelet annexin V, and PMP were significantly elevated in high-sTM patients. These findings suggest the possibility that activated platelets and cytokines participate in the pathogenesis of SLE in patients with elevated sTM levels.

Platelet transcriptional profile and protein expression in patients with systemic lupus erythematosus: up-regulation of the type I interferon system is strongly associated with vascular disease

“…This was in accordance with others who have demonstrated increased phosphatidylserine 8 and platelet-monocyte complexes 9 in patients with SLE. Despite the increased activation state of circulating platelets, we did not see any increase in platelet P-selectin expression.…”

CCN1/CYR61-mediated meticulous patrolling by Ly6C low monocytes fuels vascular inflammation

“…Interactions with monocytes and the endothelium of the vessel wall in ApoE −/− mice enable the deposition of chemokines on the cell surface and the recruitment of monocytes and thus accelerate the development of atherosclerotic plaques (58) that exhibit intense CCN1 expression (25). Platelet activation markers and soluble adhesion molecules are also observed in patients with systemic lupus erythematosus (SLE) (59). Increased recruitment of human CD16 + monocytes into synovial tissues and glomeruli is also seen in rheumatoid arthritis and lupus patients, respectively (6,(60)(61)(62)(63), and murine Ly6C low /Gr1 low monocytes are expanded in the Yaa model of SLE (14).…”

Association between mean platelet volume levels and inflammation in SLE patients presented with arthritis

“…Two studies have suggested that SLE patients have increased platelet activation 21,22 . Of these studies, Nagahama et al 22 showed that plasma platelet-derived microparticle levels were significantly higher in SLE patients than in healthy subjects.…”

“…Of these studies, Nagahama et al 22 showed that plasma platelet-derived microparticle levels were significantly higher in SLE patients than in healthy subjects. Furthermore, Nagahama et al stated 22 that MPV levels were decreased in patients with arthritis of SLE activation as in our study. Several mechanisms for how complement components interact with platelets have been proposed, and most of these theories involve platelet activation.…”