A novel and atypical NF-KB pro-inflammatory program regulated by a CamKII-proteasome axis is involved in the early activation of Muller glia by high glucose

Abstract

Key Points High glucose quickly induces an atypical NF-kB pro-inflammatory program. CamKII phosphorylation of Rpt6 subunit of the proteasome stimulates IkBα turnover and p65-p50 release. Inhibition of either CamkII or proteasome blocks this pathway.

Keywords

• Diabetic retinopathy
• Muller glia
• NF-kB pathway
• Proteasome
• CamKII