IL-8 Is an Angiogenic Factor in Human Coronary Atherectomy Tissue

Simonini, Americo; Moscucci, Mauro; Müller, D.; Bates, Eric R.; Pagani, Francis D.; Burdick, Marie D.; Strieter, Robert M.

doi:10.1161/01.cir.101.13.1519

Cited by 192 publications

(122 citation statements)

References 28 publications

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“…Recently, it has been demonstrated that IL-8 may play an important role in the development of atherosclerosis (4,10,31). Although monocytes contribute to the development of atherosclerotic lesions, IL-8 is a powerful trigger for firm adhesion of monocytes to vascular endothelium (10).…”

Section: Discussionmentioning

confidence: 99%

“…It has been recently suggested that atherosclerosis is related to inflammatory process induced by activation of proinflammatory mediators, including adhesion molecules (11) and cytokines (10,31). To induce leukocyte migration to inflamed tissue, it is essential for leukocytes to adhere to microvascular endothelium (32).…”

mentioning

confidence: 99%

“…It has been reported that ICAM-1, a member of the immunoglobulin superfamily, is required for leukocyte migration into inflamed area (3,6,35) and plays an important role in inflammatory disease, including bronchial asthma, lung injury, and ischemic heart disease (18)(19)(20)(21)(22). IL-8, a CXC chemokine that induces the migration and proliferation of endothelial cells and smooth muscle cells, is a potent angiogenic factor that may play a substantial role in atherosclerosis (4,31). Increased expression of IL-8 has been reported in atherosclerotic lesions and circulating macrophages from patients with atherosclerosis (31).…”

mentioning

confidence: 99%

“…IL-8, a CXC chemokine that induces the migration and proliferation of endothelial cells and smooth muscle cells, is a potent angiogenic factor that may play a substantial role in atherosclerosis (4,31). Increased expression of IL-8 has been reported in atherosclerotic lesions and circulating macrophages from patients with atherosclerosis (31). MCP-1 is upregulated in human atherosclerotic plaques, suggesting a role for MCP-1 in the development of early atherosclerotic lesions (5,10).…”

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confidence: 99%

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Effects of obstructive sleep apnea on circulating ICAM-1, IL-8, and MCP-1

Ohga

Tomita

Wada

et al. 2003

Journal of Applied Physiology

300

176

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structive sleep apnea syndrome (OSAS) is one of the most important risk factors of cardiovascular disorders. In the treatment of OSAS, nasal continuous positive airway pressure (nCPAP) has been widely used and found to be effective. In the present study, we hypothesized that the hypoxic stress caused by obstructive sleep apnea would increase circulating intercellular adhesion molecule-1 (ICAM-1), interleukin-8 (IL-8), and monocyte chemoattractant protein-1 (MCP-1) in untreated OSAS patients compared with an age-matched control group. In addition, we hypothesized that nCPAP may decrease OSAS-induced hypoxic stress and mediators. To examine these hypotheses, we measured circulating ICAM-1 and IL-8 before and after nCPAP therapy in OSAS patients. We observed that nCPAP decreased apnea, desaturation, and the circulating ICAM-1 and IL-8 levels in OSAS patients. The circulating levels of ICAM-1, IL-8, and MCP-1 in untreated OSAS patients were significantly greater than those in the controls. These observations suggest that nCPAP therapy could reduce OSAS-induced hypoxia and generation of inflammatory mediators. Treatment of OSAS using nCPAP can be, therefore, a potential approach to decrease risk of the progression of OSAS-associated disorders. cytokines; cardiovascular disorders; ischemic heart disease; desaturation magnitude; hypoxic stress; intracellular adhesion molecule-1; monocyte chemoattractant protein-1; interleukin-8

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Effects of obstructive sleep apnea on circulating ICAM-1, IL-8, and MCP-1

Ohga

Tomita

Wada

et al. 2003

Journal of Applied Physiology

300

176

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“…Angiogenesis has also been demonstrated within atherosclerotic plaques, and may contribute to the pathogenesis of plaque formation (70)(71)(72). The angiogenic ELR+ CXC chemokine, CXCL8, is over-expressed in human coronary artery plaque samples, as compared to control samples from internal mammary arteries without atherosclerosis, where it co-localized with factor VIII-related antigen expression on endothelial cells in the coronary atherectomy specimens, and is the major mediator of net angiogenic activity of the plaque in the rat cornea micro-pocket assay (73). A large number of chemokines are induced in the context of myocardial ischaemia and heart failure (74,75), but the specific contribution of these mediators to angiogenesis has not been clearly established.…”

Section: Chemokine-induced Angiogenesis In Inflammatory and Fibroprolmentioning

confidence: 99%

Chemokines as mediators of angiogenesis

Mehrad¹,

Keane²,

Strieter³

2007

Thromb Haemost

175

141

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SummaryChemokines were originally described as cytokines that mediate leukocyte recruitment to sites of inflammation. Members of a subgroup of chemokines, the CXC family, also play a critical role in both physiologic and pathologic angiogenesis, including in the context of chronic inflammation, fibrosis, and malignancy. A unique feature of this family of cytokines is that, on the basis of their structure and receptor binding, individual ligands display either angiogenic or angiostatic biological activity in the regulation of angiogenesis. In this review, we summarize the key literature in this growing field.

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