Reverse signaling through BAFF differentially regulates the expression of inflammatory mediators and cytoskeletal movements in THP-1 cells

Sung Tak Jeon, Won Jung Kim, Sang Min Lee, Min Young Lee, Seung Beom Park, Seung Hee Lee, In-San Kim, Kyoungho Suk, Beom Kyu Choi, Eun M. Choi, Byoung S. Kwon, Won Ha Lee

Research output: Contribution to journalArticle

33 Citations (Scopus)

Abstract

Most members of the tumor-necrosis factor superfamily have been reported to mediate reverse signaling in T cells, macrophages, and/or dendritic cells. BAFF has been reported to have important functions in B-cell survival through forward signaling, but the presence of reverse signaling has not been explored. To investigate the possibility of BAFF-mediated reverse signaling, the expression patterns and functions of BAFF were analyzed in monocytic cell lines including the human macrophage-like cell line, THP-1. The expression of BAFF and its receptors was detected in monocytic cell lines, either before or after activation. The stimulation of BAFF induced the expression of matrix metalloproteinase (MMP)-9, interleukin -8, and transforming growth factor-β-induced gene product (βig-h3) and the upregulation of intercellular adhesion molecule-1 in THP-1 cells. The activation of mitogen-activated protein kinase extracellular signal-regulated kinase1/2 and nuclear factor-κB was required for these responses. In addition to these stimulatory effects, BAFF-mediated signaling inhibited processes involving cytoskeletal movement such as phagocytosis and transmigration through blocking the activation of phosphatidylinositol 3-kinase/AKT and Rac-1. Furthermore, murine primary macrophage culture such as peritoneal macrophages expressed BAFF and stimulation of it induced the expression of MMP-9. These observations show that the reverse signaling initiated from BAFF induces the expression of inflammatory mediators while suppressing the cytoskeletal movements associated with phagocytosis and transmigration.

Original languageEnglish
Pages (from-to)148-156
Number of pages9
JournalImmunology and Cell Biology
Volume88
Issue number2
DOIs
Publication statusPublished - 2010 Feb 1
Externally publishedYes

Fingerprint

Macrophages
Matrix Metalloproteinase 9
Phagocytosis
Cell Line
B-Cell Activation Factor Receptor
Phosphatidylinositol 3-Kinase
Immunoglobulin Genes
Peritoneal Macrophages
Transforming Growth Factors
Intercellular Adhesion Molecule-1
Mitogen-Activated Protein Kinases
Interleukin-8
Dendritic Cells
Cell Survival
B-Lymphocytes
Up-Regulation
Tumor Necrosis Factor-alpha
T-Lymphocytes

Keywords

  • Atherosclerosis
  • BAFF
  • Inflammation
  • Macrophage
  • Rheumatoid arthritis
  • Signaling transduction

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Cell Biology

Cite this

Reverse signaling through BAFF differentially regulates the expression of inflammatory mediators and cytoskeletal movements in THP-1 cells. / Jeon, Sung Tak; Kim, Won Jung; Lee, Sang Min; Lee, Min Young; Park, Seung Beom; Lee, Seung Hee; Kim, In-San; Suk, Kyoungho; Choi, Beom Kyu; Choi, Eun M.; Kwon, Byoung S.; Lee, Won Ha.

In: Immunology and Cell Biology, Vol. 88, No. 2, 01.02.2010, p. 148-156.

Research output: Contribution to journalArticle

Jeon, ST, Kim, WJ, Lee, SM, Lee, MY, Park, SB, Lee, SH, Kim, I-S, Suk, K, Choi, BK, Choi, EM, Kwon, BS & Lee, WH 2010, 'Reverse signaling through BAFF differentially regulates the expression of inflammatory mediators and cytoskeletal movements in THP-1 cells', Immunology and Cell Biology, vol. 88, no. 2, pp. 148-156. https://doi.org/10.1038/icb.2009.75
Jeon, Sung Tak ; Kim, Won Jung ; Lee, Sang Min ; Lee, Min Young ; Park, Seung Beom ; Lee, Seung Hee ; Kim, In-San ; Suk, Kyoungho ; Choi, Beom Kyu ; Choi, Eun M. ; Kwon, Byoung S. ; Lee, Won Ha. / Reverse signaling through BAFF differentially regulates the expression of inflammatory mediators and cytoskeletal movements in THP-1 cells. In: Immunology and Cell Biology. 2010 ; Vol. 88, No. 2. pp. 148-156.
@article{5d5c689c8a15437385ef2f0f3024dbcb,
title = "Reverse signaling through BAFF differentially regulates the expression of inflammatory mediators and cytoskeletal movements in THP-1 cells",
abstract = "Most members of the tumor-necrosis factor superfamily have been reported to mediate reverse signaling in T cells, macrophages, and/or dendritic cells. BAFF has been reported to have important functions in B-cell survival through forward signaling, but the presence of reverse signaling has not been explored. To investigate the possibility of BAFF-mediated reverse signaling, the expression patterns and functions of BAFF were analyzed in monocytic cell lines including the human macrophage-like cell line, THP-1. The expression of BAFF and its receptors was detected in monocytic cell lines, either before or after activation. The stimulation of BAFF induced the expression of matrix metalloproteinase (MMP)-9, interleukin -8, and transforming growth factor-β-induced gene product (βig-h3) and the upregulation of intercellular adhesion molecule-1 in THP-1 cells. The activation of mitogen-activated protein kinase extracellular signal-regulated kinase1/2 and nuclear factor-κB was required for these responses. In addition to these stimulatory effects, BAFF-mediated signaling inhibited processes involving cytoskeletal movement such as phagocytosis and transmigration through blocking the activation of phosphatidylinositol 3-kinase/AKT and Rac-1. Furthermore, murine primary macrophage culture such as peritoneal macrophages expressed BAFF and stimulation of it induced the expression of MMP-9. These observations show that the reverse signaling initiated from BAFF induces the expression of inflammatory mediators while suppressing the cytoskeletal movements associated with phagocytosis and transmigration.",
keywords = "Atherosclerosis, BAFF, Inflammation, Macrophage, Rheumatoid arthritis, Signaling transduction",
author = "Jeon, {Sung Tak} and Kim, {Won Jung} and Lee, {Sang Min} and Lee, {Min Young} and Park, {Seung Beom} and Lee, {Seung Hee} and In-San Kim and Kyoungho Suk and Choi, {Beom Kyu} and Choi, {Eun M.} and Kwon, {Byoung S.} and Lee, {Won Ha}",
year = "2010",
month = "2",
day = "1",
doi = "10.1038/icb.2009.75",
language = "English",
volume = "88",
pages = "148--156",
journal = "Immunology and Cell Biology",
issn = "0818-9641",
publisher = "Nature Publishing Group",
number = "2",

}

TY - JOUR

T1 - Reverse signaling through BAFF differentially regulates the expression of inflammatory mediators and cytoskeletal movements in THP-1 cells

AU - Jeon, Sung Tak

AU - Kim, Won Jung

AU - Lee, Sang Min

AU - Lee, Min Young

AU - Park, Seung Beom

AU - Lee, Seung Hee

AU - Kim, In-San

AU - Suk, Kyoungho

AU - Choi, Beom Kyu

AU - Choi, Eun M.

AU - Kwon, Byoung S.

AU - Lee, Won Ha

PY - 2010/2/1

Y1 - 2010/2/1

N2 - Most members of the tumor-necrosis factor superfamily have been reported to mediate reverse signaling in T cells, macrophages, and/or dendritic cells. BAFF has been reported to have important functions in B-cell survival through forward signaling, but the presence of reverse signaling has not been explored. To investigate the possibility of BAFF-mediated reverse signaling, the expression patterns and functions of BAFF were analyzed in monocytic cell lines including the human macrophage-like cell line, THP-1. The expression of BAFF and its receptors was detected in monocytic cell lines, either before or after activation. The stimulation of BAFF induced the expression of matrix metalloproteinase (MMP)-9, interleukin -8, and transforming growth factor-β-induced gene product (βig-h3) and the upregulation of intercellular adhesion molecule-1 in THP-1 cells. The activation of mitogen-activated protein kinase extracellular signal-regulated kinase1/2 and nuclear factor-κB was required for these responses. In addition to these stimulatory effects, BAFF-mediated signaling inhibited processes involving cytoskeletal movement such as phagocytosis and transmigration through blocking the activation of phosphatidylinositol 3-kinase/AKT and Rac-1. Furthermore, murine primary macrophage culture such as peritoneal macrophages expressed BAFF and stimulation of it induced the expression of MMP-9. These observations show that the reverse signaling initiated from BAFF induces the expression of inflammatory mediators while suppressing the cytoskeletal movements associated with phagocytosis and transmigration.

AB - Most members of the tumor-necrosis factor superfamily have been reported to mediate reverse signaling in T cells, macrophages, and/or dendritic cells. BAFF has been reported to have important functions in B-cell survival through forward signaling, but the presence of reverse signaling has not been explored. To investigate the possibility of BAFF-mediated reverse signaling, the expression patterns and functions of BAFF were analyzed in monocytic cell lines including the human macrophage-like cell line, THP-1. The expression of BAFF and its receptors was detected in monocytic cell lines, either before or after activation. The stimulation of BAFF induced the expression of matrix metalloproteinase (MMP)-9, interleukin -8, and transforming growth factor-β-induced gene product (βig-h3) and the upregulation of intercellular adhesion molecule-1 in THP-1 cells. The activation of mitogen-activated protein kinase extracellular signal-regulated kinase1/2 and nuclear factor-κB was required for these responses. In addition to these stimulatory effects, BAFF-mediated signaling inhibited processes involving cytoskeletal movement such as phagocytosis and transmigration through blocking the activation of phosphatidylinositol 3-kinase/AKT and Rac-1. Furthermore, murine primary macrophage culture such as peritoneal macrophages expressed BAFF and stimulation of it induced the expression of MMP-9. These observations show that the reverse signaling initiated from BAFF induces the expression of inflammatory mediators while suppressing the cytoskeletal movements associated with phagocytosis and transmigration.

KW - Atherosclerosis

KW - BAFF

KW - Inflammation

KW - Macrophage

KW - Rheumatoid arthritis

KW - Signaling transduction

UR - http://www.scopus.com/inward/record.url?scp=77149145853&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=77149145853&partnerID=8YFLogxK

U2 - 10.1038/icb.2009.75

DO - 10.1038/icb.2009.75

M3 - Article

C2 - 19841639

AN - SCOPUS:77149145853

VL - 88

SP - 148

EP - 156

JO - Immunology and Cell Biology

JF - Immunology and Cell Biology

SN - 0818-9641

IS - 2

ER -