PKC-β activation inhibits IL-18-binding protein causing endothelial dysfunction and diabetic atherosclerosis.

ABSTRACT:

Aims

Clinical observations showed a correlation between accelerated atherosclerosis in diabetes and high plasmatic level of IL-18, a pro-inflammatory cytokine. IL-18 enhances the production of inflammatory cytokines and cellular adhesion molecules contributing to atherosclerotic plaque formation and instability. Previous studies indicated that protein kinase C (PKC)-β inhibition prevented macrophage-induced cytokine expression involved in diabetic (DM) atherosclerotic plaque development. However, the role of PKC-β activation on IL-18/IL-18-binding protein (IL-18BP) pathway causing endothelial dysfunction and monocyte adhesion in diabetes has never been explored.

Methods and results

Apoe(-/-) mice were rendered DM and fed with western diet containing ruboxistaurin (RBX), a PK

SUBMITTER: Durpes MC 

PROVIDER: S-EPMC6279179 | biostudies-literature | 2015 May

REPOSITORIES: biostudies-literature