The role of lectin-like oxidised low-density lipoprotein receptor-1 in vascular pathology

Shaw, Daniel J; Seese, Rachel; Ponnambalam, Sreenivasan; Ajjan, Ramzi

doi:10.1177/1479164114547704

Cited by 13 publications

(9 citation statements)

References 58 publications

(80 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…LOX-1, the main endothelial receptor of oxLDL, is responsible for the degradation of oxLDL. The binding of oxLDL to LOX-1 can activate NF-κB and then induce the expression of ICAM-1, VCAM-l, TNF-α, and IL-6, as well as MCP-l and MMP-9 levels [16,32,33]. We observed that catalpol decreased oxLDL levels in both serum and hepatic tissue and LOX-1 expression in the aorta.…”

mentioning

confidence: 58%

Amelioration by Catalpol of Atherosclerotic Lesions in Hypercholesterolemic Rabbits

Liu

Zhang

2015

Planta Med

View full text Add to dashboard Cite

The aim of the present study was to evaluate the effects of catalpol administration on atherosclerosis. Atherogenesis was induced by a high-cholesterol chow in male New Zealand White rabbits that were randomly assigned to receive atorvastatin (5 mg/kg/day), catalpol (5 mg/kg/day), or vehicle by oral gavage for 12 weeks. The rabbits were sacrificed after 12 weeks, and the thoracic aorta and serum were collected for further pathological and molecular biological analysis. Catalpol administration resulted in significantly attenuated atherosclerotic lesions. Total cholesterol, triglycerides, and low-density lipoprotein cholesterol were remarkably reduced, and high-density lipid cholesterol was elevated in the catalpol-treated group. Catalpol reduced the levels of tumor necrosis factor-α, interleukin-6, monocyte chemoattractant protein-1, soluble vascular cell adhesion molecule-1, and soluble intercellular adhesion molecule-1 in the serum, as well as vascular cell adhesion molecule-1, monocyte chemoattractant protein-1, tumor necrosis factor-α protein, inducible nitric oxide synthase, matrix metalloproteinases-9, and nuclear factor-κB protein65 in the aortic arch. In addition, catalpol treatment reduced the lipid peroxidation levels, while elevating antioxidant capacity. Catolpol pretreatment inhibited the nuclear translocation and DNA binding activity of nuclear factor-κB protein in oxygenized low-density lipoprotein-stimulated EA.hy926 cells. Furthermore, catolpol pretreatment activated nuclear factor erythroid 2-related factor 2 and upregulated the expression of its downstream antioxidant enzyme heme oxygenase. In summary, catalpol attenuated atherosclerotic lesions by the inhibition of inflammatory cytokines and oxidative stress status in a rabbit atherosclerotic model and enhanced the antioxidant capacity in oxygenized low-density lipoprotein-stimulated EA.hy926 cells. These results suggest that catalpol may be used to prevent and attenuate atherosclerosis.

show abstract

mentioning

confidence: 58%

Amelioration by Catalpol of Atherosclerotic Lesions in Hypercholesterolemic Rabbits

Liu

Zhang

2015

Planta Med

View full text Add to dashboard Cite

show abstract

“…Under acute inflammatory conditions, the lectin-like extracellular domain of LOX-1 may be released from the cell membrane into circulation as the soluble LOX-1 (sLOX-1) protein (28,29). Therefore, sLOX-1 may be considered a potential diagnostic and prognostic marker for atherosclerosis-associated events, including acute coronary syndrome (28,29). LOX-1 is the major receptor for ox-LDL uptake by ECs and induces a series of pathological processes in ECs (30).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-98 rescues proliferation and alleviates ox-LDL-induced apoptosis in HUVECs by targeting LOX-1

Chen

Wang

et al. 2017

Experimental and Therapeutic Medicine

View full text Add to dashboard Cite

Oxidized low-density lipoprotein (ox-LDL) is a major and critical mediator of atherosclerosis, and the underlying mechanism is thought to involve the ox-LDL-induced dysfunction of endothelial cells (ECs). MicroRNAs (miRNAs), which are a group of small non-coding RNA molecules that post-transcriptionally regulate the expression of target genes, have been associated with diverse cellular functions and the pathogenesis of various diseases, including atherosclerosis. miRNA-98 (miR-98) has been demonstrated to be involved in the regulation of cellular apoptosis; however, the role of miR-98 in ox-LDL-induced dysfunction of ECs and atherosclerosis has yet to be elucidated. Therefore, the present study aimed to investigate the role of miR-98 in ox-LDL-induced dysfunction of ECs and the underlying mechanism. It was demonstrated that miR-98 expression was markedly downregulated in ox-LDL-treated human umbilical vein ECs (HUVECs) and that miR-98 promoted the proliferation and alleviated apoptosis of HUVECs exposed to ox-LDL. In addition, the results demonstrated that lectin-like oxidized low-density lipoprotein receptor 1 (LOX-1) was a direct target of miR-98 in HUVECs, as indicated by a luciferase assay. The results of the present study suggested that miR-98 may inhibit the uptake of toxic ox-LDL, maintain HUVEC proliferation and protect HUVECs against apoptosis via the suppression of LOX-1.

show abstract

“…In addition to expression on endothelial cells, LOX-1 is also expressed on other cells, such as VSMCs, fibroblasts, myocardial cells, and macrophages. LOX-1 mediated signaling has been implicated in the development and progression of cardiovascular diseases 14, 27) . By interacting with ox-LOX-1, LOX-1 acts as a key regulator in activating endothelial cells, promoting the adhesion ability of monocytes to the endothelium, and altering VSMCs phenotype by increasing the levels of inflammatory chemokines and adhesion molecules, including monocyte chemotactic protein 1 (MCP-1), E-selectin, P-selectin, and vascular cell adhesion molecule-1 (VCAM-1) 28–30) .…”

Section: Discussionmentioning

confidence: 99%

Association of the LOX-1 rs1050283 Polymorphism with Risk for Atherosclerotic Cerebral Infarction and its Effect on sLOX-1 and LOX-1 Expression in a Chinese Population

Guo

Xiang

Yang

et al. 2017

J Atheroscler Thromb

View full text Add to dashboard Cite

Aims: The interaction between lectin-like oxidized low density lipoprotein (LDL) receptor-1 (LOX-1) and oxidized LDL (ox-LDL) has been viewed as an important pathogenic factor for cardiovascular diseases. This study aimed to explore the association of a functional polymorphism rs1050283 in the 3′-untranslated region of the LOX-1 gene with atherosclerotic cerebral infarction (ACI) susceptibility, and we also investigated the effects of the rs1050283 polymorphism on LOX-1 expression and serum levels of sLOX-1 in patients with ACI.Methods: A case-controlled study was performed in 526 patients with ACI and 640 healthy controls. Genotyping was performed by DNA sequencing method. Real-time PCR and Western blotting were used to determine the level of LOX-1 expression. Serum levels of sLOX-1 were quantified using ELISA according to the manufacturer's instruction.Results: The results of the present study showed that the frequency of rs1050283 T allele was significantly higher in patients with ACI than in healthy controls. We also found that the rs1050283 polymorphism T allele was associated with increased LOX-1 expression at mRNA and protein levels in patients with ACI. Furthermore, we also observed that among patients with ACI, those with the rs1050283 T allele showed an increased serum level of sLOX-1.Conclusion: Our research demonstrated that the rs1050283 T allele of LOX-1 is strongly associated with an increased risk for ACI in a Chinese population, which also affects levels of LOX-1 and sLOX-1.

show abstract

The role of lectin-like oxidised low-density lipoprotein receptor-1 in vascular pathology

Cited by 13 publications

References 58 publications

Amelioration by Catalpol of Atherosclerotic Lesions in Hypercholesterolemic Rabbits

Amelioration by Catalpol of Atherosclerotic Lesions in Hypercholesterolemic Rabbits

MicroRNA-98 rescues proliferation and alleviates ox-LDL-induced apoptosis in HUVECs by targeting LOX-1

Association of the LOX-1 rs1050283 Polymorphism with Risk for Atherosclerotic Cerebral Infarction and its Effect on sLOX-1 and LOX-1 Expression in a Chinese Population

Contact Info

Product

Resources

About