Association between Plasma Monocyte Chemoattractant Protein-1 Levels and the Extent of Atherosclerotic Peripheral Artery Disease

Abstract

Peripheral artery disease occurs at advanced ages and accounts for substantial cardiovascular morbidity and mortality. Monocyte chemoattractant protein-1 (MCP-1), a member of the cysteine-cysteine family of chemokines, is one of the cytokines involved in the pathogenesis of atherosclerosis and is also known as cysteine-cysteine chemokine ligand 2 (CCL2). The aim of the current study was to investigate the association between the extent of atherosclerotic peripheral artery disease (PAD) and the increase in MCP-1 level. Eighty consecutive patients who had undergone peripheral angiography for suspected PAD were included. Of these patients, 48 (60%) had hypertension, 23 (28.8%) had type 2 diabetes mellitus, 39 (48.8%) had a family history of coronary artery disease, 23 (28.8%) were cigarette smokers, and 42 (52.5%) had hypercholesterolemia. Angiography revealed that the peripheral arteries of the lower extremity were normal in 41 (51.3%) patients, whereas 39 (48.7%) patients had varying degrees of PAD. The patients were queried regarding age, gender, and atherosclerotic risk factors. The plasma MCP-1 levels were significantly lower in the patients without PAD than those in the patients with PAD (172.27 ± 38.05 pg/ mL vs. 200.87 ± 39.31 pg/mL, p = 0.001). Moreover, as the severity of PAD increases, MCP-1 levels also increase. Thus, the plasma MCP-1 level can be used in the diagnosis of PAD and in determining the extent of atherosclerotic PAD of the lower extremities, as in determining the extent of coronary artery disease.

Understanding the role of circulating chemokine (C-C motif) ligand 2 in patients with chronic ischemia threatening the lower extremities

“…We propose a plausible clinical impact of CCL2 in PAD because: first, the biological function of the CCL2/CCR2 pathway is its ability to induce cell migration; second, arteries with moderate atherosclerosis accumulate CCL2 in response to a variety of pro-inflammatory stimuli; and third, CCL2 may represent a potential therapeutic target. 7,14–18 We have already shown that serum CCL2 levels are consistently higher than plasma CCL2 levels and that analytical variability is significantly higher in serum. 18 This finding may alter the relevance of the observed clinical associations.…”

“…7,[14][15][16][17][18] We have already shown that serum CCL2 levels are consistently higher than plasma CCL2 levels and that analytical variability is significantly higher in serum. 18 This finding may alter the relevance of the observed clinical associations.…”

Genetic influence on femoral plaque and its relationship with carotid plaque: an international twin study

“…In this regard, several studies with different methodologies have been performed to investigate the various genes expression in patients with both subclinical and advanced femoral atherosclerosis. Upregulated genes mediate immune response, inflammation, apoptosis, stress response, phosphorylation, hemostasis, platelet activation and platelet aggregation have been demonstrated [30][31][32][33][34]. Croner et al [35] reported that most of overexpressed genes on proximal femoral artery specimens in peripheral artery disease patients were located in cytoplasm, membrane and nucleus having binding activity to nucleotides, cytoskeletal proteins, and transcription factors which genes were mainly involved in immune regulation.…”

Immunohistochemical Analysis of Paraoxonases and Chemokines in Arteries of Patients with Peripheral Artery Disease

“…CCL2 is likely to have considerable impact on PAD since the biological function of this chemokine is to induce monocyte migration and, as well, because the arteries with moderate atherosclerosis appear to accumulate CCL2 in response to a variety of pro-inflammatory stimuli [ 24 , 30 , 41 , 42 , 43 , 44 ]. Atherosclerosis is an inflammatory disease, and the consensus is that CCL2 is involved in its pathogenesis [ 45 ].…”