Involvement of TL1A and DR3 in induction of pro-inflammatory cytokines and matrix metalloproteinase-9 in atherogenesis

Yoon Joong Kang; Won Jung Kim; Hyung Uk Bae; Dong Ik Kim; Yong Bok Park; Jeong Euy Park; Byoung S. Kwon; Won Ha Lee

doi:10.1016/j.cyto.2004.12.001

Involvement of TL1A and DR3 in induction of pro-inflammatory cytokines and matrix metalloproteinase-9 in atherogenesis

Yoon Joong Kang, Won Jung Kim, Hyung Uk Bae, Dong Ik Kim, Yong Bok Park, Jeong Euy Park, Byoung S. Kwon, Won Ha Lee

Research output: Contribution to journal › Article › peer-review

76 Scopus citations

Abstract

TL1A (VEGI/TNFSF15) is the ligand for DR3 (TNFRSF12) and is a newly identified member of the tumor necrosis factor superfamily (TNFSF). Previously, DR3 has been shown to have a role in atherogenesis through stimulation of matrix degrading enzymes including matrix metalloproteinase (MMP)-9. Immunohistochemical staining of human carotid atherosclerotic plaques revealed a high-level expression of TL1A in regions rich in macrophage/foam cells. To investigate the role of TL1A and DR3 in the functioning of macrophage/foam cells in relation to atherogenesis, we have analyzed cellular events mediated by TL1A and DR3 in a human macrophage-like cell line, THP-1. Treatment of THP-1 cells with immobilized anti-DR3 monoclonal antibody in combination with IFN-γ caused induction of pro-atherogenic cytokines/chemokines such as TNF-α, monocyte chemoattractant protein (MCP)-1, and interleukin (IL)-8. Treatment of THP-1 cells with recombinant TL1A in combination with IFN-γ also caused induction of MMP-9 and IL-8. Furthermore, the expression of DR3 in peripheral blood monocytes was induced after atherogenic stimulation. These data suggest that TL1A and DR3 is involved in atherosclerosis via the induction of pro-inflammatory cytokines/chemokines and decreasing plaque stability by inducing extracellular matrix degrading enzymes.

Original language	English
Pages (from-to)	229-235
Number of pages	7
Journal	Cytokine
Volume	29
Issue number	5
DOIs	https://doi.org/10.1016/j.cyto.2004.12.001
State	Published - 7 Mar 2005

Keywords

Atherosclerosis
Foam cells
Matrix metalloproteinase
Monocyte
Tumor necrosis factor superfamily

Access to Document

10.1016/j.cyto.2004.12.001

Cite this

@article{9b76072c99e24f6697a7f1b077d155c8,

title = "Involvement of TL1A and DR3 in induction of pro-inflammatory cytokines and matrix metalloproteinase-9 in atherogenesis",

abstract = "TL1A (VEGI/TNFSF15) is the ligand for DR3 (TNFRSF12) and is a newly identified member of the tumor necrosis factor superfamily (TNFSF). Previously, DR3 has been shown to have a role in atherogenesis through stimulation of matrix degrading enzymes including matrix metalloproteinase (MMP)-9. Immunohistochemical staining of human carotid atherosclerotic plaques revealed a high-level expression of TL1A in regions rich in macrophage/foam cells. To investigate the role of TL1A and DR3 in the functioning of macrophage/foam cells in relation to atherogenesis, we have analyzed cellular events mediated by TL1A and DR3 in a human macrophage-like cell line, THP-1. Treatment of THP-1 cells with immobilized anti-DR3 monoclonal antibody in combination with IFN-γ caused induction of pro-atherogenic cytokines/chemokines such as TNF-α, monocyte chemoattractant protein (MCP)-1, and interleukin (IL)-8. Treatment of THP-1 cells with recombinant TL1A in combination with IFN-γ also caused induction of MMP-9 and IL-8. Furthermore, the expression of DR3 in peripheral blood monocytes was induced after atherogenic stimulation. These data suggest that TL1A and DR3 is involved in atherosclerosis via the induction of pro-inflammatory cytokines/chemokines and decreasing plaque stability by inducing extracellular matrix degrading enzymes.",

keywords = "Atherosclerosis, Foam cells, Matrix metalloproteinase, Monocyte, Tumor necrosis factor superfamily",

author = "Kang, {Yoon Joong} and Kim, {Won Jung} and Bae, {Hyung Uk} and Kim, {Dong Ik} and Park, {Yong Bok} and Park, {Jeong Euy} and Kwon, {Byoung S.} and Lee, {Won Ha}",

year = "2005",

month = mar,

day = "7",

doi = "10.1016/j.cyto.2004.12.001",

language = "English",

volume = "29",

pages = "229--235",

journal = "Cytokine",

issn = "1043-4666",

publisher = "Academic Press",

number = "5",

}

TY - JOUR

T1 - Involvement of TL1A and DR3 in induction of pro-inflammatory cytokines and matrix metalloproteinase-9 in atherogenesis

AU - Kang, Yoon Joong

AU - Kim, Won Jung

AU - Bae, Hyung Uk

AU - Kim, Dong Ik

AU - Park, Yong Bok

AU - Park, Jeong Euy

AU - Kwon, Byoung S.

AU - Lee, Won Ha

PY - 2005/3/7

Y1 - 2005/3/7

N2 - TL1A (VEGI/TNFSF15) is the ligand for DR3 (TNFRSF12) and is a newly identified member of the tumor necrosis factor superfamily (TNFSF). Previously, DR3 has been shown to have a role in atherogenesis through stimulation of matrix degrading enzymes including matrix metalloproteinase (MMP)-9. Immunohistochemical staining of human carotid atherosclerotic plaques revealed a high-level expression of TL1A in regions rich in macrophage/foam cells. To investigate the role of TL1A and DR3 in the functioning of macrophage/foam cells in relation to atherogenesis, we have analyzed cellular events mediated by TL1A and DR3 in a human macrophage-like cell line, THP-1. Treatment of THP-1 cells with immobilized anti-DR3 monoclonal antibody in combination with IFN-γ caused induction of pro-atherogenic cytokines/chemokines such as TNF-α, monocyte chemoattractant protein (MCP)-1, and interleukin (IL)-8. Treatment of THP-1 cells with recombinant TL1A in combination with IFN-γ also caused induction of MMP-9 and IL-8. Furthermore, the expression of DR3 in peripheral blood monocytes was induced after atherogenic stimulation. These data suggest that TL1A and DR3 is involved in atherosclerosis via the induction of pro-inflammatory cytokines/chemokines and decreasing plaque stability by inducing extracellular matrix degrading enzymes.

AB - TL1A (VEGI/TNFSF15) is the ligand for DR3 (TNFRSF12) and is a newly identified member of the tumor necrosis factor superfamily (TNFSF). Previously, DR3 has been shown to have a role in atherogenesis through stimulation of matrix degrading enzymes including matrix metalloproteinase (MMP)-9. Immunohistochemical staining of human carotid atherosclerotic plaques revealed a high-level expression of TL1A in regions rich in macrophage/foam cells. To investigate the role of TL1A and DR3 in the functioning of macrophage/foam cells in relation to atherogenesis, we have analyzed cellular events mediated by TL1A and DR3 in a human macrophage-like cell line, THP-1. Treatment of THP-1 cells with immobilized anti-DR3 monoclonal antibody in combination with IFN-γ caused induction of pro-atherogenic cytokines/chemokines such as TNF-α, monocyte chemoattractant protein (MCP)-1, and interleukin (IL)-8. Treatment of THP-1 cells with recombinant TL1A in combination with IFN-γ also caused induction of MMP-9 and IL-8. Furthermore, the expression of DR3 in peripheral blood monocytes was induced after atherogenic stimulation. These data suggest that TL1A and DR3 is involved in atherosclerosis via the induction of pro-inflammatory cytokines/chemokines and decreasing plaque stability by inducing extracellular matrix degrading enzymes.

KW - Atherosclerosis

KW - Foam cells

KW - Matrix metalloproteinase

KW - Monocyte

KW - Tumor necrosis factor superfamily

UR - http://www.scopus.com/inward/record.url?scp=14744279915&partnerID=8YFLogxK

U2 - 10.1016/j.cyto.2004.12.001

DO - 10.1016/j.cyto.2004.12.001

M3 - Article

C2 - 15760679

AN - SCOPUS:14744279915

SN - 1043-4666

VL - 29

SP - 229

EP - 235

JO - Cytokine

JF - Cytokine

IS - 5

ER -

Involvement of TL1A and DR3 in induction of pro-inflammatory cytokines and matrix metalloproteinase-9 in atherogenesis

Abstract

Keywords

Access to Document

Other files and links

Fingerprint

Cite this