June 2013
Volume 54, Issue 15
Free
ARVO Annual Meeting Abstract  |   June 2013
MicroRNA-15a Is Involved In Ceramide Inflammatory Pathways by Targeting the Acid Sphingomyelinase (ASM) In Diabetic retina
Author Affiliations & Notes
  • Qi Wang
    Physiology, Michigan State University, East Lansing, MI
  • Svetlana Bozack
    Physiology, Michigan State University, East Lansing, MI
  • Maria Grant
    Pharmacology and Therapeutics, University of Florida, Gainesville, FL
  • Michael Boulton
    Anatomy and Cell Biology, University of Florida, Gainesville, FL
  • Walter Esselman
    Microbiology and Molecular Genetics, Michigan State University, East Lansing, MI
  • Julia Busik
    Physiology, Michigan State University, East Lansing, MI
  • Footnotes
    Commercial Relationships Qi Wang, None; Svetlana Bozack, None; Maria Grant, None; Michael Boulton, None; Walter Esselman, None; Julia Busik, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2013, Vol.54, 3692. doi:
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      Qi Wang, Svetlana Bozack, Maria Grant, Michael Boulton, Walter Esselman, Julia Busik; MicroRNA-15a Is Involved In Ceramide Inflammatory Pathways by Targeting the Acid Sphingomyelinase (ASM) In Diabetic retina. Invest. Ophthalmol. Vis. Sci. 2013;54(15):3692.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose: MicroRNAs (miRNAs) regulate gene expression at the posttranscriptional level through translational repression and/or target messenger RNAs degradation in a sequence-dependent manner and modulate several cellular processes. Acid sphingomyelinase (ASM) is important early responder in inflammatory cytokine signaling that catalyze the hydrolysis of sphingomyelin to the proinflammatory and proapoptotic second messenger ceramide. Here, we investigated the role of miR-15a, an ASM-targeting miRNA in diabetes.

Methods: Type 1 STZ-induced diabetic mice and age matched controls were used. Mice were sacrificed and their retinas were harvested for RNA analysis. The human retinal pigment epithelial cell line ARPE-19 cultured under normal and elevated glucose conditions and the human retinal vascular endothelial cells (HREC) from diabetic (n=6) and control donors (n=6) were collected for analysis. The mRNA expressions of miR-15a, ASM, VEGF-A, VEGF-C were measured. ASM, VEGF-A, VEGF-C, NF-κB protein levels with or without miR-15a mimic or antagomir transfection were examined. The ceramide immunofluorescence intensity with or without miR-15a mimic or antagomir transfection was detected. A luciferase assay was performed to detect miR-15a’s binding to ASM 3'-untranslated region (UTR). In situ hybridization was used to localize retinal miR-15a.

Results: ASM is a predicted target of miR-15a. We demonstrated that miR-15a directly binds to ASM 3'-UTR in luciferase binding assay. miR-15a messenger RNA expression was decreased in the retinas from type 1 STZ-induced diabetic mice compared with control mice. HREC isolated from diabetic donors and ARPE-19 cells treated with 25 mmol/L glucose had decreased miR-15a expression and increased ASM expression compared with non-diabetic 5 mmol/L glucose treated cells. Delivery of miR-15a mimic in ARPE-19 cells suppressed the expression levels of ASM, VEGF-A, VEGF-C, NF-κB and ceramide production, while miR-15a antagomir transfection caused ASM, VEGF-A, VEGF-C, NF-κB and ceramide upregulation.

Conclusions: The results of this study demonstrate that dowregulation of miR-15a in diabetic retina contributes to diabetes-induced upregulation of ASM and thus pathogenesis of diabetic retinopathy.

Keywords: 499 diabetic retinopathy • 583 lipids • 557 inflammation  
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