Abstract
BackgroundAngiogenesis plays a central role in the pathophysiology of rheumatic diseases. Patients with psoriatic arthritis (PsA) demonstrate increased vascularity over patients with rheumatoid arthritis (RA), with unknown mechanisms.MethodsWe evaluated the serum levels of several pro- and anti-angiogenic factors in 62 PsA patients with active disease, 39 PsA patients in remission, 33 active RA patients, and 33 healthy controls (HC). Additionally, we used an in vitro co-culture system of fibroblast (HT1080) and monocytic-like (MM6) cell lines, to evaluate how their interactions affect the secretion of angiogenic factors and angiogenesis promoting abilities using scratch and tube formation assays.ResultsPsA patients, regardless of disease activity, exhibited higher levels of EMMPRIN/CD147, IL-17, and TNF-α relative to RA patients or HC. Factors, such as IL-6, and the ratio between CD147 and thrombospondin-1, exhibited elevated levels in active PsA patients relative to PsA patients in remission. Secretion of CD147, VEGF, and MMP-9 was increased in vitro. CD147 neutralization with an antibody reduced these levels and the ability of endothelial cells to form tube-like structures or participate in wound healing.ConclusionsCD147 plays a role in mediating angiogenesis in PsA, and the therapeutic possibilities of neutralizing it merit further investigation.
Highlights
Angiogenesis plays a central role in the pathophysiology of rheumatic diseases
Disease activity for psoriatic arthritis (PsA) patients was determined by the minimal disease activity (MDA) score [23] and the DAPSA score [24]: 39 patients were classified in remission (MDA score ≥ 5), or remission (22 patients) and low disease activity (17 patients) according to the DAPSA score
Angiogenesis is an important component in the pathophysiology of rheumatic diseases, but it has been described to be more enhanced in PsA than in rheumatoid arthritis (RA) patients [3], the molecular mechanisms that regulate this phenomenon are still unclear
Summary
Angiogenesis plays a central role in the pathophysiology of rheumatic diseases. Patients with psoriatic arthritis (PsA) demonstrate increased vascularity over patients with rheumatoid arthritis (RA), with unknown mechanisms. Angiogenesis is mostly studied in the tumoral context, it is demonstrated in rheumatic diseases to different degrees and has been implicated in. Hypoxia increases the expression of many proangiogenic factors, such as vascular endothelial growth factor (VEGF) [6], which is a strong chemoattractant for macrophages [7]. Macrophages and other infiltrating immune cells secrete enhanced levels of proinflammatory cytokines and chemokines in the inflamed synovium, such as interleukin-1β (IL-1β), IL-6, IL-8, IL17, interferon β (IFN-β), monocyte chemoattractant protein 1 (MCP-1), and tumor necrosis factor α (TNF-α) that help recruit leukocytes to sites of inflammation [8]. IL-17 and TNF-α are crucial as pro-angiogenic factors, and because they induce the expression of many MMPs that play a role in cartilage erosion and degradation [9, 10]
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