Inflammatory cytokines regulate endothelial cell survival and tissue repair functions via NF-κB signaling

Nobuhiro Kanaji, Tadashi Sato, Amy Nelson, Xingqi Wang, Yingji Li, Miok Kim, Masanori Nakanishi, Hesham E Basma, Joel Michalski, Maha Farid, Michael Chandler, William Pease, Amol N Patil, Stephen I. Rennard, Xiang-de Liu

Research output: Contribution to journalArticle

15 Scopus citations

Abstract

Inflammation contributes to the development of fibrotic and malignant diseases. We assessed the ability of inflammatory cytokines to modulate endothelial cell survival and functions related to tissue repair/remodeling. Treatment with interleukin (IL)-1β or tumor necrosis factor (TNF)-α (2 ng/mL) led to human pulmonary artery endothelial cells becoming spindle-shaped fibroblast-like cells. However, immunoblot and DNA microarray showed no change in most endothelial and mesenchymal markers. In the presence of IL-1β or TNF-α,cells were resistant to apoptosis induced by deprivation of serum and growth factor, and were more migratory. In addition, cells treated with IL-1β or TNF-α contracted collagen gels more robustly. In contrast, transforming growth factor-β1 did not induce these responses. RNA interference targeting nuclear factor (NF)-κB p65 blocked the effects of IL-1β or TNF-α on cell morphologic change, survival, migration, and collagen gel contraction. These results suggest that endothelial cells may contribute to tissue repair/remodeling via the NF-κB signaling in a milieu of airway inflammation.

Original languageEnglish (US)
Pages (from-to)127-138
Number of pages12
JournalJournal of Inflammation Research
Volume4
Issue number1
Publication statusPublished - Dec 22 2011

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Keywords

  • Apoptosis
  • IL-1β
  • NF-κB
  • TNF-α
  • Tissue repair

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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