Upregulation of OLR1 and IL17A genes and their association with blood glucose and lipid levels in femoropopliteal artery disease

Abstract

Abstract. Oxidized low-density lipoprotein receptor 1 (OLR1) and interleukin 17A (IL17A) have pro-inflammatory roles in the development of cardiovascular disorders. The present study evaluated the association of OLR1 and IL17A and their polymorphisms with the development of femoropopliteal (FP) artery disease. The mRNA expression of OLR1 and IL17A in peripheral blood mononuclear cells as well as the frequency of OLR1 rs11053646 and IL17A rs8193037 and rs3819025 polymorphisms were assessed by polymerase chain reaction in 70 patients with FP artery disease and 80 age-matched disease-free controls. Furthermore, the levels of plasma cytokines were assessed by multiplex immunoassay. OLR1 and IL17A mRNA expression was significantly higher in patients with FP artery disease compared with that in controls (P<0.001). No significant difference was observed in the genotypic frequencies of OLR1 rs11053646 (P= 0.87) or in IL17A rs8193037 and rs3819025 (P= 0.80 and 0.92, respectively) polymorphisms between patients with FP artery disease and controls. Plasma IL4, -6, -10, -22, -31 and -33 as well as soluble cluster of differentiation 40 ligand and tumor necrosis factor-α levels were significantly increased among FP artery disease patients compared with controls (P<0.05). Furthermore, OLR1 expression was positively correlated with triglyceride (r= 0.463, P<0.001), low-density lipoprotein cholesterol (r= 0.507, P<0.001) and total cholesterol levels (r= 0.357, P= 0.006) in patients with FP artery disease. To the best of our knowledge, the present study was the first to identify an association between OLR1 and IL17A genes and FP artery disease. OLR1 and IL17A mRNA transcripts may be associated with blood lipid parameters and with the development of FP artery disease.

Associations of Common Genetic Variants on <i>IL-17</i> Genes and Carotid Intima-Media Thickness

“…Furthermore, only very few IL-17-positive cells were observed in the opposite normal hemispheres of human brains 26 ) . Similarly, several research groups observed IL-17A were expressed in human atherosclerotic lesions 27 – 31 ) and correlated the IL-17A expression levels with the vulnerability of atherosclerotic lesions 28 , 29 ) . On the contrarily, one study reported that IL-17A expression was associated with more stable plaque phenotype rather than macrophage rich plaque areas 32 ) .…”

“…Similarly, studies of serum or plasma levels of circulating IL-17A and severity or vulnerability of atherosclerosis showed inconsistent results. Most of studies had shown higher levels of circulating IL-17A in subjects with unstable or more advanced plaques 31 – 36 ) . Unexpectedly, a prospective, multicenter study that enrolled acute ST-elevation and non-ST-elevation MI patients found that lower serum IL17 levels correlated with significantly higher risks of all-cause mortality and recurrent MI 40 ) .…”

Prognostic model of 10 immune-related genes and identification of small molecule drugs in bladder urothelial carcinoma (BLCA)

“…AHNAK is a giant structural nucleoprotein involved in diverse biological process including muscle membrane repair, blood-brain barrier, and cell proliferation and migration (35)(36)(37)(38). As to OLR1, a lectin-like scavenger receptor, it was mainly expressed in vascular cells and vasculature-rich organs (39), and could function as inflammation promotor in atherogenesis (40). Coincidently, RAC3 could promote ox-LDL induced endothelial dysfunction (41).…”

The transcriptome of CMML monocytes is highly inflammatory and reflects leukemia-specific and age-related alterations

“…42 Oxidized low-density lipoprotein receptor-1 (OLR-1), is a type II transmembrane receptor of the C-type lectin family that induces oxidative stress, activates tumor necrosis factor a TNFa/nuclear factor-kB (NFkB), upregulates the expression of monocyte chemoattractant protein-1 (MCP1), a key mediator of inflammatory processes, and has a proinflammatory role in cardiovascular disease. [43][44][45] calcium/calmodulin-dependent protein kinase kinase 2 (CAMKK2) transcripts were downregulated in CMML CD14 1 monocytes. As previous studies have demonstrated, a crucial role of the CAMKK2-59-AMP-activated protein kinase catalytic subunit-1 (PRKAA1) axis in the differentiation of monocytes into macrophages, our data are consistent with the observation that the differentiation from monocytes to macrophages is compromised in CMML.…”