Immune complexes suppressed autophagy in glomerular endothelial cells

Linlin Wang, Ka Wai Helen Law

Research output: Journal article publicationJournal articleAcademic researchpeer-review

6 Citations (Scopus)

Abstract

Lupus nephritis is an immune-complexes mediated glomerulonephritis. Vascular lesions and endothelial cell injuries are common in lupus nephritis and important for renal damage. However, the precise mechanisms by which immune complexes lead to endothelial cell injuries are still unclear. Autophagy is a conserved metabolic process and shows protective roles in many cell types and diseases. In present study, we investigated whether immune complexes could affect autophagy and participate in endothelial dysfunctions. Heat-aggregated gamma globulin (HAGG) was used to substitute immune complexes. Glomerular endothelial cells (GECs) were incubated with HAGG and autophagy-related markers were evaluated. Results showed that HAGG suppressed autophagy in GECs, through Akt/mTOR-dependent pathway. The combination of HAGG and tumor necrosis factor-alpha suppressed autophagy in GECs and further decreased cell viabilities. The suppressed effects of HAGG on GECs autophagy and viability, especially under inflammatory microenvironment, may provide new views for explaining the mechanisms of renal impairments in lupus nephritis.

Original languageEnglish
Pages (from-to)1-8
Number of pages8
JournalCellular Immunology
Volume328
DOIs
Publication statusPublished - 1 Jun 2018

Keywords

  • Autophagy
  • Glomerular endothelial cell
  • Heat-aggregated gamma globulin
  • Lupus nephritis

ASJC Scopus subject areas

  • Immunology

Cite this