Erythropoietin increases circulating endothelial progenitor cells and reduces the formation and progression of cerebral aneurysm in rats

Xu, Yi; Tian, Yikui; Wei, Huijie; Chen, J.; Dong, Jing; Zacharek, Alex; Zhang, J.-N.

doi:10.1016/j.neuroscience.2011.02.051

Cited by 46 publications

(31 citation statements)

References 38 publications

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“…Evidence indicates that number and function of circulating EPCs correlate inversely with cardiovascular risk factors [26]. Our previous studies also demonstrated that the number and potential of EPCs were closely related to CA formation [11,14]. Although the efficacy of aspirin in cardiovascular disease has been reported, few studies have investigated the effect of aspirin on the number and function of EPCs.…”

Section: Discussionmentioning

confidence: 94%

“…7-week-old male Sprague-Dawley rats were obtained from Military Medical Academy of China. CA induction was performed as previously described [14,16]. Briefly, animals were anesthetized with 10 % chloral hydrate (0.3 ml/ 100 g, i.p.)…”

Section: Preparation Of Ca Model and Experimental Groupsmentioning

confidence: 99%

“…Circulating EPCs were examined using flow cytometry according to our previous study [14]. Briefly, 1.5 ml whole blood (n = 6/group) was collected through the retro-orbital venous plexus and mononuclear cells (MNCs) were isolated using a Ficoll gradient centrifugation method.…”

Section: Assessment Of Circulating Epcs Levelmentioning

confidence: 99%

“…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].…”

Section: Introductionmentioning

confidence: 99%

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Aspirin Inhibits Degenerative Changes of Aneurysmal Wall in a Rat Model

Wang

Tian

et al. 2015

Neurochem Res

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Aneurysmal subarachnoid hemorrhage still has a high mortality and morbidity despite notable advances in surgical approaches to cerebral aneurysm (CA). We examined the role of aspirin in vascular inflammation and degeneration. CA was induced in male Sprague-Dawley rats by ligating left common carotid artery and bilateral posterior renal arteries with or without aspirin treatment. The right anterior cerebral artery/olfactory artery (ACA/OA) bifurcations were stripped and assessed morphologically after Verhoeff's Van Gieson staining. Blood sample was obtained to examine circulating CD34(+) CD133(+) endothelial progenitor cells (EPCs), platelet aggregation and platelet counts. Macrophages infiltration in aneurysmal wall was evaluated by immunohistochemistry. Expression of matrix metalloproteinase-2 and 9 (MMP-2 and 9), nuclear factor kappa B (NF-κB), macrophage chemoattractant protein-1 (MCP-1) and vascular cell adhesion molecule-1 (VCAM-1) was examined by RT-PCR. 2 months after CA induction, surgically treated rats manifested aneurysmal degeneration in ACA/OA bifurcations. Aspirin-treated rats exhibited a significant decrease in degradation of internal elastic lamina (IEL), medial layer thinning, CA size and macrophages infiltration with reduced expression of MMP-2 and 9 compared with rats in the CA group. RT-PCR demonstrated that the upregulation of NF-κB, MCP-1 and VCAM-1 after CA induction was reversed by aspirin treatment. Aspirin treatment following CA induction increased circulating EPCs to near control levels and reduced platelet aggregation without changing platelet counts. The evidence suggested that aspirin significantly reduced degeneration of aneurysm walls by inhibiting macrophages-mediated chronic inflammation and mobilizing EPCs.

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Section: Discussionmentioning

confidence: 94%

Section: Preparation Of Ca Model and Experimental Groupsmentioning

confidence: 99%

Section: Assessment Of Circulating Epcs Levelmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Aspirin Inhibits Degenerative Changes of Aneurysmal Wall in a Rat Model

Wang

Tian

et al. 2015

Neurochem Res

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“…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).…”

Section: Changes In Constituents Of the Cerebral Blood Vessel Wall Inmentioning

confidence: 99%

Biology of Intracranial Aneurysms: Role of Inflammation

Chalouhi

Ali

Jabbour

et al. 2012

J Cereb Blood Flow Metab

430

418

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Intracranial aneurysms (IAs) linger as a potentially devastating clinical problem. Despite intense investigation, our understanding of the mechanisms leading to aneurysm development, progression and rupture remain incompletely defined. An accumulating body of evidence implicates inflammation as a critical contributor to aneurysm pathogenesis. Intracranial aneurysm formation and progression appear to result from endothelial dysfunction, a mounting inflammatory response, and vascular smooth muscle cell phenotypic modulation producing a pro-inflammatory phenotype. A later final common pathway appears to involve apoptosis of cellular constituents of the vessel wall. These changes result in degradation of the integrity of the vascular wall leading to aneurysmal dilation, progression and eventual rupture in certain aneurysms. Various aspects of the inflammatory response have been investigated as contributors to IA pathogenesis including leukocytes, complement, immunoglobulins, cytokines, and other humoral mediators. Furthermore, gene expression profiling of IA compared with control arteries has prominently featured differential expression of genes involved with immune response/inflammation. Preliminary data suggest that therapies targeting the inflammatory response may have efficacy in the future treatment of IA. Further investigation, however, is necessary to elucidate the precise role of inflammation in IA pathogenesis, which can be exploited to improve the prognosis of patients harboring IA.

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