title: Inflammatory cytokines regulate endothelial cell survival and tissue repair functions via NF-κB signaling.
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.
authors.affiliation: Division of Hematology, Rheumatology and Respiratory Medicine, Kagawa University, Kagawa, Japan.
authors.forename: Nobuhiro
authors.initials: N
authors.lastname: Kanaji
authors.forename: Tadashi
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authors.forename: Amy
authors.initials: A
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authors.forename: Xingqi
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authors.forename: Yingji
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authors.lastname: Li
authors.forename: Miok
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authors.lastname: Kim
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authors.lastname: Nakanishi
authors.forename: Hesham
authors.initials: H
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authors.lastname: Patil
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authors.initials: SI
authors.lastname: Rennard
authors.forename: Xiangde
authors.initials: X
authors.lastname: Liu
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