Your browser doesn't support javascript.
loading
Diabetes enhances translation of Cd40 mRNA in murine retinal Müller glia via a 4E-BP1/2-dependent mechanism.
Dierschke, Sadie K; Toro, Allyson L; Miller, William P; Sunilkumar, Siddharth; Dennis, Michael D.
Afiliación
  • Dierschke SK; Department of Cellular and Molecular Physiology, Pennsylvania State College of Medicine, Hershey, Pennsylvania, USA.
  • Toro AL; Department of Cellular and Molecular Physiology, Pennsylvania State College of Medicine, Hershey, Pennsylvania, USA.
  • Miller WP; Department of Cellular and Molecular Physiology, Pennsylvania State College of Medicine, Hershey, Pennsylvania, USA.
  • Sunilkumar S; Department of Cellular and Molecular Physiology, Pennsylvania State College of Medicine, Hershey, Pennsylvania, USA.
  • Dennis MD; Department of Cellular and Molecular Physiology, Pennsylvania State College of Medicine, Hershey, Pennsylvania, USA mdennis@psu.edu.
J Biol Chem ; 295(31): 10831-10841, 2020 07 31.
Article en En | MEDLINE | ID: mdl-32475820
Activation of the immune costimulatory molecule cluster of differentiation 40 (CD40) in Müller glia has been implicated in the initiation of diabetes-induced retinal inflammation. Results from previous studies support that CD40 protein expression is elevated in Müller glia of diabetic mice; however, the mechanisms responsible for this increase have not been explored. Here, we evaluated the hypothesis that diabetes augments translation of the Cd40 mRNA. Mice receiving thiamet G (TMG), an inhibitor of the O-GlcNAc hydrolase O-GlcNAcase, exhibited enhanced retinal protein O-GlcNAcylation and increased Cd40 mRNA translation. TMG administration also promoted Cd40 mRNA association with Müller cell-specific ribosomes isolated from the retina of RiboTag mice. Similar effects on O-GlcNAcylation and Cd40 mRNA translation were also observed in the retina of a mouse model of type 1 diabetes. In cultured cells, TMG promoted sequestration of the cap-binding protein eIF4E (eukaryotic translation in initiation factor 4E) by 4E-BP1 (eIF4E-binding protein 1) and enhanced cap-independent Cd40 mRNA translation as assessed by a bicistronic reporter that contained the 5'-UTR of the Cd40 mRNA. Ablation of 4E-BP1/2 prevented the increase in Cd40 mRNA translation in TMG-exposed cells, and expression of a 4E-BP1 variant that constitutively sequesters eIF4E promoted reporter activity. Extending on the cell culture results, we found that in contrast to WT mice, diabetic 4E-BP1/2-deficient mice did not exhibit enhanced retinal Cd40 mRNA translation and failed to up-regulate expression of the inflammatory marker nitric-oxide synthase 2. These findings support a model wherein diabetes-induced O-GlcNAcylation of 4E-BP1 promotes Cd40 mRNA translation in Müller glia.
Asunto(s)
Palabras clave

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Biosíntesis de Proteínas / ARN Mensajero / Proteínas de Ciclo Celular / Antígenos CD40 / Factores Eucarióticos de Iniciación / Proteínas Adaptadoras Transductoras de Señales / Diabetes Mellitus Experimental / Diabetes Mellitus Tipo 1 / Células Ependimogliales Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: J Biol Chem Año: 2020 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Biosíntesis de Proteínas / ARN Mensajero / Proteínas de Ciclo Celular / Antígenos CD40 / Factores Eucarióticos de Iniciación / Proteínas Adaptadoras Transductoras de Señales / Diabetes Mellitus Experimental / Diabetes Mellitus Tipo 1 / Células Ependimogliales Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: J Biol Chem Año: 2020 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Estados Unidos