The role of FoxO1 in interleukin-1β-induced autostimulation in retina endothelial cells and retinas of diabetic rats

Microvasc Res. 2017 Jul:112:93-100. doi: 10.1016/j.mvr.2017.03.003. Epub 2017 Mar 7.

Abstract

Diabetic retinopathy is a chronic, low-grade inflammatory disease. The present study aimed to investigate the effect of forkhead transcription factor O1 (FoxO1) expression on interleukin-1β (IL-1β)-induced autostimulation, both in vitro in human retina microvascular endothelial cells (HRMECs), and in vivo in retinas isolated from streptozotocin-induced diabetic rats. High-glucose (HG) and recombinant IL-1β treatment were both shown to increase the expression of FoxO1 and IL-1β in HRMECs in a dose-dependent manner. IL-1 receptor antagonist (IL-1RA) and mitogen-activated protein kinase (MAPK) inhibitors reduced IL-1β-induced expression of FoxO1 in HRMECs. Moreover, the increased expressions of FoxO1 and IL-1β in the retinas of diabetic rats were significantly decreased by intravitreal injection of lentiviral vector-mediated FoxO1 small-interfering RNA. Together, these results suggest that HG triggers IL-1β synthesis in HRMECs. The produced IL-1β induces increased FoxO1 expression, as well as interacts with the IL-1 receptor to activate MAPK signaling and thereby induces IL-1β autostimulation. The IL-1β-induced autostimulation can be inhibited by downregulation of FoxO1, accompanied by a reduction of inflammation. Together, these findings identify novel functions for FoxO1 and IL-1β in diabetic retinopathy.

Keywords: Autostimulation; Diabetic retinopathy; Forkhead transcription factor O1; Inflammation; Interleukin-1β.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Autocrine Communication* / drug effects
  • Blood Glucose / metabolism
  • Cells, Cultured
  • Diabetes Mellitus, Experimental / genetics
  • Diabetes Mellitus, Experimental / metabolism*
  • Diabetes Mellitus, Experimental / pathology
  • Diabetic Retinopathy / genetics
  • Diabetic Retinopathy / metabolism*
  • Diabetic Retinopathy / pathology
  • Endothelial Cells / drug effects
  • Endothelial Cells / metabolism*
  • Endothelial Cells / ultrastructure
  • Forkhead Box Protein O1 / genetics
  • Forkhead Box Protein O1 / metabolism*
  • Humans
  • Interleukin-1beta / genetics
  • Interleukin-1beta / metabolism*
  • Interleukin-1beta / pharmacology
  • Male
  • Mitogen-Activated Protein Kinases / metabolism
  • Nerve Tissue Proteins / genetics
  • Nerve Tissue Proteins / metabolism*
  • RNA Interference
  • Rats, Sprague-Dawley
  • Receptors, Interleukin-1 / metabolism
  • Retina / drug effects
  • Retina / metabolism*
  • Retina / ultrastructure
  • Retinal Vessels / drug effects
  • Retinal Vessels / metabolism*
  • Retinal Vessels / ultrastructure
  • Signal Transduction
  • Transfection
  • Up-Regulation

Substances

  • Blood Glucose
  • FOXO1 protein, human
  • Forkhead Box Protein O1
  • IL1B protein, human
  • IL1B protein, rat
  • Interleukin-1beta
  • Nerve Tissue Proteins
  • Receptors, Interleukin-1
  • Foxo1 protein, rat
  • Mitogen-Activated Protein Kinases