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https://eyecro.com

  • AboutUs_Normal-24 The EyeCRO Approach
    • About Us
    • Careers
    • Location
    • Partners
  • MiDrops MiDROPS™
  • InVivo Models
    • Allergic Conjunctivitis
    • Corneal Sensitivity
    • Corneal Wound Healing
    • Diabetic Keratopathy
    • DL-AAA Retinal Leakage
    • Dry Eye Disease
    • Endotoxin induced Uveitis
    • Experimental Autoimmune Uveitis
    • Geographic Atrophy
    • Inherited Retinal Degenerations
    • Ischemia Reperfusion Injury
    • Laser-induced Choroidal Neovascularization
    • Light Damaged
    • Mitochondrial Neuropathy
    • Optic Nerve Crush
    • Oxygen Induced Retinopathy
    • Retinal Detachment
    • Retinal Vein Occlusion
    • STZ-induced Diabetic Retinopathy
    • VEGF-induced permeability
  • InVitro Capabilities
    • A2E Quantification
    • Bioanalytical Detection
    • Biochemistry
    • Histology
    • Ophthalmic Imaging and Physiology
  • News News
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Preclinical Ophthalmic Contract Research

Serum retinol-binding protein-induced endothelial inflammation is mediated through the activation of toll-like receptor 4

April 17, 2017 //  by stanselb

“Retinol-binding protein 4 (RBP4) is a novel adipokine (adipose-derived cytokine) that is clinically associated with obesity, insulin resistance, type 2 diabetes (T2DM), and cardiovascular disease. In addition, patients with proliferative diabetic retinopathy (DR) have increased serum RBP4 levels compared to diabetic patients with mild or no retinopathy, which raises the possibility that RBP4 is somehow involved in the pathogenesis of DR. We demonstrated previously that RBP4 elevation induces inflammation in primary human retinal microvascular endothelial cells (HRECs) and human umbilical vein endothelial cells (HUVECs) by increasing the expression of proinflammatory cytokines, chemokines, and adhesion molecules, including interleukin 6 (IL-6), monocyte chemoattractant protein (MCP-1), endothelial cell selectin (E-selectin), vascular cell adhesion molecule 1 (VCAM-1), and intracellular adhesion molecule 1 (ICAM-1). We have also shown that RBP4-induced endothelial inflammation is retinol independent and involves activation of nuclear factor κB (NF-κB). In the present study, we used HRECs as a model system to learn more about the cell receptor and signaling pathways that modulate the proinflammatory activity of RBP4.”

Read the entire paper here.

 

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