Mechanical injury and IL-1β regulated LOXs and MMP-1, 2, 3 expression in ACL fibroblasts co-cultured with synoviocytes.
Adult
Anterior Cruciate Ligament
/ cytology
Anterior Cruciate Ligament Injuries
/ metabolism
Cellular Microenvironment
Coculture Techniques
Female
Fibroblasts
/ cytology
Humans
Interleukin-1beta
/ metabolism
Male
Matrix Metalloproteinases, Secreted
/ metabolism
Middle Aged
Protein-Lysine 6-Oxidase
/ metabolism
Synoviocytes
/ cytology
Crosstalk
Inflammation
Mechanical injury
Microenvironment
Journal
Biotechnology letters
ISSN: 1573-6776
Titre abrégé: Biotechnol Lett
Pays: Netherlands
ID NLM: 8008051
Informations de publication
Date de publication:
Aug 2020
Aug 2020
Historique:
received:
25
04
2019
accepted:
20
03
2020
pubmed:
3
5
2020
medline:
9
2
2021
entrez:
3
5
2020
Statut:
ppublish
Résumé
Interleukin (IL)-1β in the joint cavity increases to promote healing after anterior cruciate ligament (ACL) injury. Synovial tissue is a major joint microenvironmental regulator after ACL injury. The purpose of this study was to investigate the effects of synovial cells (SCs) on lysyl oxidase (LOX) and matrix metalloproteinase (MMP) production by ACL fibroblasts (ACLfs) in the presence of IL-1β. This study sheds light on the regulation of LOX and MMP-1, -2, -3 expression by ACLfs co-cultured with SCs and treated with IL-1β. LOX and MMP-1, 2, 3 gene/protein expression in IL-1β/stretch-stimulated ACLfs co-cultured with SCs were measured by real-time quantitative PCR and Western blot. Meanwhile, MMP-2 activity was analyzed by zymogram. The results showed that co-culture with SCs increased LOX and MMP-1, -2, -3 gene and protein expression in the presence of IL-1β. Next, ACLfs were subjected to 12% mechanical stretch to simulate pathological injury. Under these conditions, SCs inhibited IL-1β-mediated upregulation of LOXs. However, IL-1β enhanced the expression of MMP-1, -2, -3 in injured ACLfs. SCs can either inhibit or increase LOX production in the presence of IL-1β, while promoting the accumulation of MMP in injured ACLfs. These results may provide crucial insights into the mechanisms underlying ACL poor healing capacity after injury.
Identifiants
pubmed: 32358726
doi: 10.1007/s10529-020-02870-9
pii: 10.1007/s10529-020-02870-9
doi:
Substances chimiques
IL1B protein, human
0
Interleukin-1beta
0
LOX protein, human
EC 1.4.3.13
Protein-Lysine 6-Oxidase
EC 1.4.3.13
Matrix Metalloproteinases, Secreted
EC 3.4.24.-
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
1567-1579Subventions
Organisme : National Natural Science Foundation of China
ID : 11532004
Organisme : National Natural Science Foundation of China
ID : 11832008
Organisme : National Natural Science Foundation of China
ID : 11602181
Organisme : National Natural Science Foundation of China
ID : 11802096
Organisme : National Natural Science Foundation of China
ID : 11902058
Organisme : Innovation and Attracting Talents Program for College and University (''111'' Project)
ID : B06023
Organisme : China Postdoctoral Science Foundation
ID : 2018M630867
Organisme : Visiting Scholar Foundation of Key Laboratory of Biorheological Science and Technology (Chongqing University), Ministry of Education
ID : CQKLBST-2018-006
Organisme : Visiting Scholar Foundation of Key Laboratory of Biorheological Science and Technology (Chongqing University), Ministry of Education
ID : CQKLBST-2018-009
Organisme : Sharing fund of Chongqing university's large-scale equipment
ID : 2009063038