title: MicroRNA-126 contributes to Niaspan treatment induced vascular restoration after diabetic retinopathy.
abstract: Diabetic retinopathy (DR) is a serious microvascular complication of diabetes and a major cause of blindness in the developing world. Early diabetic retinopathy is characterized by a loss of pericytes and vascular endothelial cells, a breakdown of the blood-retinal barrier, vascular dysfunction and vascular-neuroinflammation. However, optimal treatment options and related mechanisms are still unclear. MicroRNA-126 (miR-126) plays a potential role in the pathogenesis in DR, which may regulate VEGF, Ang-1 and VCAM-1 expressions. This study investigated the therapeutic effects and mechanisms of Niaspan treatment of DR in diabetes (DM) rats. DM rats exhibits significantly decreased miR-126 and tight junction Claudin-5/Occludin/ZO-1 genes expression, and increased Blood retinal-barrier (BRB) breakdown, retinal apoptosis and VEGF/VEGFR, as well as VCAM-1/CD45 expressions in the retina compared to normal control group. Niaspan treatment significantly improved clinical and histopathological outcomes; decreased the expressions of VEGF/VEGFR, VCAM-1/CD45, apoptosis and BRB breakdown, significantly increased tight junction proteins and Ang-1/Tie-2 expressions, as well as increased retinal miR-126 expression compared to non-treatment diabetic rats. These data are the first to show that Niaspan treatment ameliorates DR through its repair vascular and inhibits inflammatory effects, and also suggest that the miR-126 pathway may contribute to Niaspan treatment induced benefit effects.
authors.affiliation: Department of Ophthalmology, Tianjin Medical University General Hospital, No. 154, Anshan Road, Tianjin, 300052, China.
authors.forename: Yang
authors.initials: Y
authors.lastname: Wang
authors.affiliation: Department of Ophthalmology, Tianjin Medical University General Hospital, No. 154, Anshan Road, Tianjin, 300052, China.
authors.forename: Hua
authors.initials: H
authors.lastname: Yan
mesh_terms: D043925:Angiogenesis Inducing Agents / Q000008:administration & dosage*; D042501:Angiogenic Proteins / Q000235:genetics / Q000378:metabolism; D000818:Animals; D017209:Apoptosis; D001205:Ascorbic Acid; D001786:Blood Glucose; D002478:Cells, Cultured; D002762:Cholecalciferol; D002784:Cholesterol / Q000097:blood; D003687:Dehydroepiandrosterone / Q000031:analogs & derivatives; D003692:Delayed-Action Preparations; D003921:Diabetes Mellitus, Experimental / Q000097:blood / Q000150:complications*; D003930:Diabetic Retinopathy / Q000097:blood / Q000188:drug therapy* / Q000235:genetics / Q000378:metabolism; D004353:Drug Evaluation, Preclinical; D015870:Gene Expression / Q000187:drug effects; D006801:Humans; D000960:Hypolipidemic Agents / Q000008:administration & dosage; D008297:Male; D035683:MicroRNAs / Q000502:physiology*; D009525:Niacin / Q000008:administration & dosage*; D009539:Nicotinic Acids; D010936:Plant Extracts; D034622:RNA Interference; D017208:Rats, Wistar; D012160:Retina / Q000187:drug effects / Q000378:metabolism; D012171:Retinal Vessels / Q000187:drug effects; D062725:Tight Junction Proteins / Q000378:metabolism; D019108:Tight Junctions / Q000378:metabolism
chemical_list: D043925:Angiogenesis Inducing Agents; D042501:Angiogenic Proteins; D001786:Blood Glucose; D003692:Delayed-Action Preparations; C524255:HUM 5007; D000960:Hypolipidemic Agents; C571458:MIRN126 microRNA, rat; D035683:MicroRNAs; D009539:Nicotinic Acids; D010936:Plant Extracts; D062725:Tight Junction Proteins; D002762:Cholecalciferol; D009525:Niacin; D003687:Dehydroepiandrosterone; D002784:Cholesterol; D001205:Ascorbic Acid