Changes and function of circulating endothelial progenitor cells in patients with cerebral aneurysm

Abstract

Endothelial dysfunction is a trigger for the formation of cerebral aneurysm (CA). The circulating endothelial progenitor cell (EPC) plays an important role in postnatal vasculogenesis and reduction of endothelial injury. In this study, we tested the hypothesis that decreased number and impaired function of circulating EPCs correlate with CA formation in patients. Blood circulating EPCs were identified by flow cytometry. The level of plasma vascular endothelial growth factor (VEGF) was measured by ELISA. Circulating EPCs from patients (n = 27) were cultured in vitro, and the function of EPCs was evaluated by cell migration and senescence-associated β-galactosidase activity. The number of circulating EPCs was significantly decreased in both unruptured and ruptured CA patients compared with healthy control subjects. Impaired migratory capacity and elevated cellular senescence of cultured EPCs were observed in patients with CA (ruptured and unruptured). The percentages of EPC senescence in patients with CAs were significantly and negatively correlated with the number of circulating EPCs. In addition, there were higher levels of plasma VEGF in CA patients compared with healthy control subjects. Our results show that the numbers and functions of circulating EPCs are reduced in patients with CAs. These findings suggest that the decreased number and impaired function of circulating EPCs in CA patients may contribute to the pathophysiological process of aneurysm formation.

Biology of Intracranial Aneurysms: Role of Inflammation

“…A healthy endothelium has antiatherogenic properties and promotes vasodilation while inhibiting platelet aggregation and adhesion, smooth muscle proliferation, and leukocyte adherence/pro-inflammatory cascades (Dumont et al, 2001a(Dumont et al, ,b, 2003b. Endothelial dysfunction and pathophysiological changes in the endothelium may be the inciting event in IA formation (Tamura et al, 2009;Wei et al, 2011;Xu et al, 2011). The potential importance of the role of the endothelium in IA pathology is highlighted by the fact that a susceptibility locus for IA formation in certain populations is found on chromosome 8q in a region that is Intracranial aneurysms and inflammation N Chalouhi et al required for formation and maintenance of endothelial cells (Bilguvar et al, 2008).…”

Aspirin Inhibits Degenerative Changes of Aneurysmal Wall in a Rat Model

“…Endothelial progenitor cells (EPCs) play a critical role in neovasculogenesis and maintenance of vascular integrity [11][12][13]. Our previous study showed that the circulating level of EPCs was reduced in CA patients and rats, which correlates with the pathogenesis of CA [11,14]. Aspirin has been reported to increase the proangiogenic potential of EPCs [15].…”

“…However, the precise protective mechanism has not been clarified in their studies and there is no direct experimental evidence supporting the epidemiologic findings. Endothelial progenitor cells (EPCs) play a critical role in neovasculogenesis and maintenance of vascular integrity [11][12][13]. Our previous study showed that the circulating level of EPCs was reduced in CA patients and rats, which correlates with the pathogenesis of CA [11,14].…”

Nonsteroidal Anti-Inflammatory Drugs: A Potential Pharmacological Treatment for Intracranial Aneurysm

“…An early feature of IA is dysfunction and degradation of ECs, as evidenced by functional and morphological changes [35]. EC health and function relies upon a balance between the degree of endothelial damage and the body’s repair capacity.…”

“…Injury to the vascular wall stimulates the release of endothelial progenitor cells (EPCs), which are a subpopulation of hematopoietic stem cells that have the ability to proliferate, migrate, and differentiate into ECs thus playing a critical role in vascular repair [36, 37]. Patients at risk for vascular disease have fewer circulating EPCs, decreased EPC migration, and increased senescence compared to healthy controls, suggesting that these patients have impaired ability to repair vessel wall damage [35, 38]. …”