Inflammation by activated macrophage-like THP-1 cells increases human dura mater cell adhesion with alteration of integrin α2β1 and matrix metalloproteinase

Kyuha Chong, Woo Keun Kwon, Joo-Han Kim, Youn-Kwan Park, Wonki Yoon, Jong Hyun Kim, Taek-Hyun Kwon, Hong Joo Moon

Research output: Contribution to journalArticle

Abstract

This study was designed to investigate (i) extracellular matrix to specify adhesive substrates to human dura mater cell (hDMC); (ii) the alteration on adhesion-related molecules in hDMC; and (iii) secreted matrix metalloproteinases (MMPs) linked with extracellular matrix remodeling after exposure to inflammation. The hDMC was cultured from human dura mater tissue, and the studies were performed with hDMC after co-culturing with macrophage like THP-1 cells (Mϕ). The adhesion of co-cultured hDMC through collagen I increased 6.4-fold and through collagen IV increased 5.0-fold compared with the adhesion of naïve cells (p < 0.001). Integrin subtype α2β1 expression was increased 6.3-fold (p < 0.001) and α1 expression was decreased 2.0-fold (p < 0.001) in the co-cultured cells compared with the naïve cells. Co-culturing induced significant increases in MMP-1 (13.9-fold, p < 0.01), MMP-3 (7.6-fold, p < 0.01), and VEGF (VEGF: 3.8-fold, p < 0.05) expression and decreases in MMP-9 (0.1-fold, p < 0.01) compared with the sum of naïve hDMC and Mϕ values. Increased hDMC adhesion under inflammatory conditions is caused by an increased cellular affinity for collagen I and IV mediated by increased hDMC levels of integrin subtype α2β1 and environmental MMP-1, -3 and decreased MMP-9. Selective integrin subtype α2β1 inhibition assay showed 37.8% and 35.7% reduction in adhesion of co-cultured hDMC to collagen I (p < 0.001) and IV (p = 0.057), respectively. The present study provides insight into the pathological conditions related to dura mater adhesion in inflammation.

Original languageEnglish
JournalJournal of Orthopaedic Research
DOIs
Publication statusAccepted/In press - 2019 Jan 1

Fingerprint

Dura Mater
Matrix Metalloproteinases
Cell Adhesion
Integrins
Macrophages
Inflammation
Collagen
Matrix Metalloproteinase 3
Matrix Metalloproteinase 1
Matrix Metalloproteinase 9
Vascular Endothelial Growth Factor A
Extracellular Matrix
Cultured Cells
Secreted Matrix Metalloproteinases
Adhesives

Keywords

  • cell adhesion
  • dura mater
  • extracellular matrix
  • inflammation
  • integrin
  • matrix metalloproteinase

ASJC Scopus subject areas

  • Orthopedics and Sports Medicine

Cite this

@article{3192125441f24e82aa773e58e16bb4ed,
title = "Inflammation by activated macrophage-like THP-1 cells increases human dura mater cell adhesion with alteration of integrin α2β1 and matrix metalloproteinase",
abstract = "This study was designed to investigate (i) extracellular matrix to specify adhesive substrates to human dura mater cell (hDMC); (ii) the alteration on adhesion-related molecules in hDMC; and (iii) secreted matrix metalloproteinases (MMPs) linked with extracellular matrix remodeling after exposure to inflammation. The hDMC was cultured from human dura mater tissue, and the studies were performed with hDMC after co-culturing with macrophage like THP-1 cells (Mϕ). The adhesion of co-cultured hDMC through collagen I increased 6.4-fold and through collagen IV increased 5.0-fold compared with the adhesion of na{\"i}ve cells (p < 0.001). Integrin subtype α2β1 expression was increased 6.3-fold (p < 0.001) and α1 expression was decreased 2.0-fold (p < 0.001) in the co-cultured cells compared with the na{\"i}ve cells. Co-culturing induced significant increases in MMP-1 (13.9-fold, p < 0.01), MMP-3 (7.6-fold, p < 0.01), and VEGF (VEGF: 3.8-fold, p < 0.05) expression and decreases in MMP-9 (0.1-fold, p < 0.01) compared with the sum of na{\"i}ve hDMC and Mϕ values. Increased hDMC adhesion under inflammatory conditions is caused by an increased cellular affinity for collagen I and IV mediated by increased hDMC levels of integrin subtype α2β1 and environmental MMP-1, -3 and decreased MMP-9. Selective integrin subtype α2β1 inhibition assay showed 37.8{\%} and 35.7{\%} reduction in adhesion of co-cultured hDMC to collagen I (p < 0.001) and IV (p = 0.057), respectively. The present study provides insight into the pathological conditions related to dura mater adhesion in inflammation.",
keywords = "cell adhesion, dura mater, extracellular matrix, inflammation, integrin, matrix metalloproteinase",
author = "Kyuha Chong and Kwon, {Woo Keun} and Joo-Han Kim and Youn-Kwan Park and Wonki Yoon and Kim, {Jong Hyun} and Taek-Hyun Kwon and Moon, {Hong Joo}",
year = "2019",
month = "1",
day = "1",
doi = "10.1002/jor.24207",
language = "English",
journal = "Journal of Orthopaedic Research",
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T1 - Inflammation by activated macrophage-like THP-1 cells increases human dura mater cell adhesion with alteration of integrin α2β1 and matrix metalloproteinase

AU - Chong, Kyuha

AU - Kwon, Woo Keun

AU - Kim, Joo-Han

AU - Park, Youn-Kwan

AU - Yoon, Wonki

AU - Kim, Jong Hyun

AU - Kwon, Taek-Hyun

AU - Moon, Hong Joo

PY - 2019/1/1

Y1 - 2019/1/1

N2 - This study was designed to investigate (i) extracellular matrix to specify adhesive substrates to human dura mater cell (hDMC); (ii) the alteration on adhesion-related molecules in hDMC; and (iii) secreted matrix metalloproteinases (MMPs) linked with extracellular matrix remodeling after exposure to inflammation. The hDMC was cultured from human dura mater tissue, and the studies were performed with hDMC after co-culturing with macrophage like THP-1 cells (Mϕ). The adhesion of co-cultured hDMC through collagen I increased 6.4-fold and through collagen IV increased 5.0-fold compared with the adhesion of naïve cells (p < 0.001). Integrin subtype α2β1 expression was increased 6.3-fold (p < 0.001) and α1 expression was decreased 2.0-fold (p < 0.001) in the co-cultured cells compared with the naïve cells. Co-culturing induced significant increases in MMP-1 (13.9-fold, p < 0.01), MMP-3 (7.6-fold, p < 0.01), and VEGF (VEGF: 3.8-fold, p < 0.05) expression and decreases in MMP-9 (0.1-fold, p < 0.01) compared with the sum of naïve hDMC and Mϕ values. Increased hDMC adhesion under inflammatory conditions is caused by an increased cellular affinity for collagen I and IV mediated by increased hDMC levels of integrin subtype α2β1 and environmental MMP-1, -3 and decreased MMP-9. Selective integrin subtype α2β1 inhibition assay showed 37.8% and 35.7% reduction in adhesion of co-cultured hDMC to collagen I (p < 0.001) and IV (p = 0.057), respectively. The present study provides insight into the pathological conditions related to dura mater adhesion in inflammation.

AB - This study was designed to investigate (i) extracellular matrix to specify adhesive substrates to human dura mater cell (hDMC); (ii) the alteration on adhesion-related molecules in hDMC; and (iii) secreted matrix metalloproteinases (MMPs) linked with extracellular matrix remodeling after exposure to inflammation. The hDMC was cultured from human dura mater tissue, and the studies were performed with hDMC after co-culturing with macrophage like THP-1 cells (Mϕ). The adhesion of co-cultured hDMC through collagen I increased 6.4-fold and through collagen IV increased 5.0-fold compared with the adhesion of naïve cells (p < 0.001). Integrin subtype α2β1 expression was increased 6.3-fold (p < 0.001) and α1 expression was decreased 2.0-fold (p < 0.001) in the co-cultured cells compared with the naïve cells. Co-culturing induced significant increases in MMP-1 (13.9-fold, p < 0.01), MMP-3 (7.6-fold, p < 0.01), and VEGF (VEGF: 3.8-fold, p < 0.05) expression and decreases in MMP-9 (0.1-fold, p < 0.01) compared with the sum of naïve hDMC and Mϕ values. Increased hDMC adhesion under inflammatory conditions is caused by an increased cellular affinity for collagen I and IV mediated by increased hDMC levels of integrin subtype α2β1 and environmental MMP-1, -3 and decreased MMP-9. Selective integrin subtype α2β1 inhibition assay showed 37.8% and 35.7% reduction in adhesion of co-cultured hDMC to collagen I (p < 0.001) and IV (p = 0.057), respectively. The present study provides insight into the pathological conditions related to dura mater adhesion in inflammation.

KW - cell adhesion

KW - dura mater

KW - extracellular matrix

KW - inflammation

KW - integrin

KW - matrix metalloproteinase

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