Endothelial Progenitor Cells as a Marker of Endothelial Dysfunction and Atherosclerosis in Ankylosing Spondylitis: A Cross-Sectional Study

Abstract

Endothelial progenitor cells (EPCs) have reparative potential in overcoming the endothelial dysfunction and reducing cardiovascular risk. EPC depletion has been demonstrated in the setting of established atherosclerotic diseases. We evaluated whether reduced EPCs population are associated with endothelial dysfunction, subclinical atherosclerosis, and inflammatory markers in ankylosing spondylitis (AS) patients without any known traditional cardiovascular risk factor. We performed a cross-sectional study of 30 consecutive AS patients and 25 age- and sex-matched healthy controls. Patients with traditional cardiovascular risk factors were excluded. Circulating EPCs (CD34/CD133) were quantified by flow cytometry. The assessment of endothelial function by brachial artery flow-mediated dilatation (FMD) and ultrasound assessment of carotid intima-media thickness (CIMT) was measured in both the groups. EPCs cells were significantly (0.020 ± 0.001 vs. 0.040 ± 0.010%, < 0.001) reduced in patients with AS compared with healthy controls. Endothelial function (7.35 ± 2.54 vs. 10.27 ± 1.73, = 0.002), CIMT (0.63 ± 0.01 vs. 0.35 ± 0.02, < 0.001), and inflammatory markers were also significantly ( < 0.01) altered as compared with controls. EPCs inversely correlated with tumor necrosis factor (TNF)-α and C-reactive protein (CRP) and positively correlated with endothelial function. Present study results demonstrate depleted EPC population in AS patients compared with controls. Increased level of CRP and TNF-α appears to play a key role in EPC depletion and the latter contributes to endothelial dysfunction and atherosclerosis in AS. EPC population would, therefore, represent an attractive measure of endothelial dysfunction and accelerated atherosclerosis disease associated with AS.

VCAM-1 expression is upregulated by CD34+/CD133+-stem cells derived from septic patients

“…Assuming, that homing of vascular progenitor cells in sepsis involves various mediators that recruit them to activated endothelium in response to a damage-induced inflammation, we set out to determine in septic patients which adhesion molecules are expressed by CD34 + /CD133 + -stem cells—containing vascular progenitors [ 17 , 18 ]—and could therefore be involved in the CD34 + /CD133 + -stem cell-driven repair process. Furthermore, we wanted to analyse, if the upregulation of adhesion molecules by CD34 + /CD133 + -stem cells is associated with survival or mortality of septic patients.…”

Traditional and Non-Traditional Risk Factors Involved with Endothelial Dysfunction and Arterial Stiffness in Autoimmune Rheumatic Diseases

“…Several studies have shown arterial stiffness in patient's large arteries [11] [12]. To our knowledge, the studies have not demonstrated an increase in the common (carotid intima-media thickness) cIMT [11]. Moreover, no studies have evaluated the PWV.…”

“…The literature contains less information about the assessment of endothelial function in AS [11] [12]. Several studies have shown arterial stiffness in patient's large arteries [11] [12].…”

“…Regarding FMD, an important impairment was shown [12]. The possible mechanism involved was related to impairments in the anti-atherogenic factors linked to high density protein [11] [12], but limited studies have elucidated the potential mechanism involved the vascular dysfunction of these patients.…”

Обґрунтування Необхідності Й Оцінка Ефективності Корекції Ендотеліальної Дисфункції В пацієнтів З Анкілозивним Спондилоартритом

“…Тривале запалення призводить до активації та пошкодження ендотелію, є причиною атерогенезу (Taurog J.D. et al, 2016;Verma I. et al, 2017) і розвит ку гострих серцево-судинних станів, при яких атеросклеротична бляшка дестабілізується і розривається, що призводить до тромбоутворення (Teupser D. et al, 2011). Саме тому запалення набуває особливого значення в розвитку ЕД та серцево-судинної патології в пацієнтів з автоімунними захворюваннями, постійним атрибутом яких є власне персистуюче системне запалення (Syngle A. et al, 2010).…”