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 Citations (Scopus)

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
StatePublished - Dec 22 2011

Fingerprint

Interleukin-1
Endothelium
Cell Survival
Endothelial Cells
Tumor Necrosis Factor-alpha
Cytokines
Collagen
Gels
Inflammation
Transforming Growth Factors
RNA Interference
Oligonucleotide Array Sequence Analysis
Pulmonary Artery
Intercellular Signaling Peptides and Proteins
Fibroblasts
Apoptosis
Survival
Serum

Keywords

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

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

Cite this

Inflammatory cytokines regulate endothelial cell survival and tissue repair functions via NF-κB signaling. / Kanaji, Nobuhiro; Sato, Tadashi; Nelson, Amy; Wang, Xingqi; Li, Yingji; Kim, Miok; Nakanishi, Masanori; Basma, Hesham E; Michalski, Joel; Farid, Maha; Chandler, Michael; Pease, William; Patil, Amol N; Rennard, Stephen I.; Liu, Xiang-de.

In: Journal of Inflammation Research, Vol. 4, No. 1, 22.12.2011, p. 127-138.

Research output: Contribution to journalArticle

Kanaji, N, Sato, T, Nelson, A, Wang, X, Li, Y, Kim, M, Nakanishi, M, Basma, HE, Michalski, J, Farid, M, Chandler, M, Pease, W, Patil, AN, Rennard, SI & Liu, X 2011, 'Inflammatory cytokines regulate endothelial cell survival and tissue repair functions via NF-κB signaling', Journal of Inflammation Research, vol. 4, no. 1, pp. 127-138.
Kanaji, Nobuhiro ; Sato, Tadashi ; Nelson, Amy ; Wang, Xingqi ; Li, Yingji ; Kim, Miok ; Nakanishi, Masanori ; Basma, Hesham E ; Michalski, Joel ; Farid, Maha ; Chandler, Michael ; Pease, William ; Patil, Amol N ; Rennard, Stephen I. ; Liu, Xiang-de. / Inflammatory cytokines regulate endothelial cell survival and tissue repair functions via NF-κB signaling. In: Journal of Inflammation Research. 2011 ; Vol. 4, No. 1. pp. 127-138.
@article{b32f66b8b42c489682012648ff0f0098,
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.",
keywords = "Apoptosis, IL-1β, NF-κB, TNF-α, Tissue repair",
author = "Nobuhiro Kanaji and Tadashi Sato and Amy Nelson and Xingqi Wang and Yingji Li and Miok Kim and Masanori Nakanishi and Basma, {Hesham E} and Joel Michalski and Maha Farid and Michael Chandler and William Pease and Patil, {Amol N} and Rennard, {Stephen I.} and Xiang-de Liu",
year = "2011",
month = "12",
day = "22",
language = "English (US)",
volume = "4",
pages = "127--138",
journal = "Journal of Inflammation Research",
issn = "1178-7031",
publisher = "Dove Medical Press Ltd.",
number = "1",

}

TY - JOUR

T1 - Inflammatory cytokines regulate endothelial cell survival and tissue repair functions via NF-κB signaling

AU - Kanaji, Nobuhiro

AU - Sato, Tadashi

AU - Nelson, Amy

AU - Wang, Xingqi

AU - Li, Yingji

AU - Kim, Miok

AU - Nakanishi, Masanori

AU - Basma, Hesham E

AU - Michalski, Joel

AU - Farid, Maha

AU - Chandler, Michael

AU - Pease, William

AU - Patil, Amol N

AU - Rennard, Stephen I.

AU - Liu, Xiang-de

PY - 2011/12/22

Y1 - 2011/12/22

N2 - 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.

AB - 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.

KW - Apoptosis

KW - IL-1β

KW - NF-κB

KW - TNF-α

KW - Tissue repair

UR - http://www.scopus.com/inward/record.url?scp=83755228719&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=83755228719&partnerID=8YFLogxK

M3 - Article

AN - SCOPUS:83755228719

VL - 4

SP - 127

EP - 138

JO - Journal of Inflammation Research

JF - Journal of Inflammation Research

SN - 1178-7031

IS - 1

ER -