CCAAT/enhancer binding protein delta (CEBPD) elevating PTX3 expression inhibits macrophage-mediated phagocytosis of dying neuron cells

Chiung Yuan Ko, Ling Hua Chang, Yi Chao Lee, Esta Sterneck, Chun Pei Cheng, Shun Hua Chen, A. Mei Huang, Joseph T. Tseng, Ju Ming Wang

Research output: Contribution to journalArticlepeer-review

43 Citations (Scopus)

Abstract

The CCAAT/enhancer binding protein delta (CEBPD, C/EBPδ, NF-IL6β) is induced in many inflammation-related diseases, suggesting that CEBPD and its downstream targets may play central roles in these conditions. Neuropathological studies show that a neuroinflammatory response parallels the early stages of Alzheimer's disease (AD). However, the precise mechanistic correlation between inflammation and AD pathogenesis remains unclear. CEBPD is upregulated in the astrocytes of AD patients. Therefore, we asked if activation of astrocytic CEBPD could contribute to AD pathogenesis. In this report, a novel role of CEBPD in attenuating macrophage-mediated phagocytosis of damaged neuron cells was found. By global gene expression profiling, we identified the inflammatory marker pentraxin-3 (PTX3, TNFAIP5, TSG-14) as a CEBPD target in astrocytes. Furthermore, we demonstrate that PTX3 participates in the attenuation of macrophage-mediated phagocytosis of damaged neuron cells. This study provides the first demonstration of a role for astrocytic CEBPD and the CEBPD-regulated molecule PTX3 in the accumulation of damaged neurons, which is a hallmark of ADpathogenesis.

Original languageEnglish
Pages (from-to)422.e11-422.e25
JournalNeurobiology of Aging
Volume33
Issue number2
DOIs
Publication statusPublished - 2012 Feb

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)
  • Ageing
  • Developmental Biology
  • Clinical Neurology
  • Geriatrics and Gerontology

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