Biochemical and Biophysical Research Communications
Expression of lectin-like oxidized LDL receptor-1 in smooth muscle cells after vascular injury
Section snippets
Methods
Rabbit aorta model. Male Japanese white rabbits weighing 3.0–3.5 kg were used and all surgical procedures on rabbits were carried out under general anesthesia with sodium pentobarbital (40 mg/kg), ketamine (2 mg/kg), and xylazine (8 mg/kg). The balloon-injury model of the rabbit aorta was created as reported previously [9]. At various time points (6, 12, and 24 h, 2, 5, and 7 days, and 2, 4, 8, 16, and 24 weeks after balloon injury), animals were anesthetized with sodium pentobarbital (40 mg/kg),
Vascular injury model of the rabbit aorta
We used a balloon-injury model of rabbit aorta in which LOX-1 mRNA and protein expression levels were analyzed at 6, 12, and 24 h, 2, 5, and 7 days, and 2, 4, 8, 16, and 24 weeks after the balloon injury. Neointima appeared 5 days after balloon injury and the neointimal area increased until 8 weeks (data not shown). We have previously shown that not only media, but also the neointima, are composed predominantly of SMC based on immunohistochemical staining for muscle actin [9].
Time course of LOX-1 mRNA expression
Based on RT-PCR
Discussion
In this study, we demonstrated that LOX-1 mRNA and protein are induced and persistently expressed in neointimal and medial SMC of the rabbit aorta for 24 weeks after balloon injury. LOX-1 protein is similarly expressed in restenotic lesions after balloon-angioplasty in humans. In cell culture experiments, the chemical inhibitor of LOX-1 reduced the SMC proliferation stimulated by relatively low concentrations of ox-LDL which was hard to induce apoptosis, although previous studies have shown
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LOX-1 Receptor: A Diagnostic Tool and Therapeutic Target in Atherogenesis
2024, Current Problems in CardiologyCritical Role of LOX-1-PCSK9 Axis in the Pathogenesis of Atheroma Formation and Its Instability
2021, Heart Lung and CirculationCitation Excerpt :CD36 is required by nonclassical monocytes to effectively patrol the endothelium during early atherogenesis to limit inflammation and atheroma formation [57]. Similarly, LOX-1 is expressed on the cell membranes of vascular smooth muscle cells (VSMCs) and is upregulated by proinflammatory cytokines, such as TNF-α, interleukin-1 (IL-1) and interferon-gamma (INF-y) [58]. Binding of ox-LDL to LOX-1 stimulates the migration and proliferation of VSMCs.
Contribution of lectin-like oxidized low-density lipoprotein receptor-1 and LOX-1 modulating compounds to vascular diseases
2018, Vascular PharmacologyCitation Excerpt :Blocking LOX-1 reduced oxLDL-induced production of hyaluronan in smooth muscles, protecting these cells from migration and adherence of monocytes to extracellular matrix [108]. Furthermore, LOX-1 has an important role in neointimal formation after vascular injury; during the progression of vascular injury, LOX-1 expression gradually shifts from cells in the media to the intima [16,106,109]. Platelets adhere to a dysfunctional endothelium and promote smooth muscle proliferation and migration [2,3].
Dual signaling evoked by oxidized LDLs in vascular cells
2017, Free Radical Biology and MedicineCitation Excerpt :All these factors contribute to the recruitment and adhesion of monocytes to the activated endothelium, their penetration in the intima, their differentiation into macrophages and the formation of foam cells [103]. LOX-1 plays a crucial role in the biphasic signaling evoked by oxLDLs, particularly in the dual effect of oxLDLs on NF-κB [104], angiogenesis [105,106], SMC proliferation [107] or apoptosis [108]. LOX-1 stimulates adaptive, protective and antioxidant responses, mediated by the nuclear factor E2-related factor 2 (Nrf2) and the antioxidant stress protein heme oxygenase 1 (HO-1) in SMCs [109] and in endothelial cells [110].