RAGE-dependent NF-kB inflammation processes in the capsule of frozen shoulders.
Adult
Aged
Bursitis
/ metabolism
Case-Control Studies
Female
Gene Expression
HMGB1 Protein
/ genetics
Humans
Immunohistochemistry
Ligaments, Articular
/ metabolism
Male
Middle Aged
NF-kappa B
/ genetics
Real-Time Polymerase Chain Reaction
Receptor for Advanced Glycation End Products
/ genetics
Retrospective Studies
Signal Transduction
Toll-Like Receptor 2
/ genetics
Toll-Like Receptor 4
/ genetics
Frozen shoulder
advanced glycation end-products
gene expression
high-mobility group box 1
nuclear factor-kappa B
receptor of advanced glycation end-products
Journal
Journal of shoulder and elbow surgery
ISSN: 1532-6500
Titre abrégé: J Shoulder Elbow Surg
Pays: United States
ID NLM: 9206499
Informations de publication
Date de publication:
Sep 2020
Sep 2020
Historique:
received:
13
09
2019
revised:
30
12
2019
accepted:
01
01
2020
pubmed:
14
4
2020
medline:
14
1
2021
entrez:
14
4
2020
Statut:
ppublish
Résumé
The etiology of frozen shoulder (FS) remains uncertain. Advanced glycation end-products (AGEs) cause the cross-linking and stabilization of collagen and are increased in FS. The purpose of this study was to elucidate the pathogenesis of FS by evaluating the receptor of AGE (RAGE)-dependent pathways. Tissue samples of the coracohumeral ligament (CHL) and anterior inferior glenohumeral ligament (IGHL) were collected from 33 patients with FS, with severe stiffness, and 25 with rotator cuff tears (RCTs) as controls. Gene expression levels of RAGE, high-mobility group box 1 (HMGB1), Toll-like receptor 2 (TLR2), TLR4, nuclear factor-kappa B (NF-kB), and cytokines were evaluated using a quantitative real-time polymerase chain reaction. The immunoreactivities of carboxymethyllysine (CML), pentosidine, and RAGE were also evaluated. CML and pentosidine were further evaluated using high-performance liquid chromatography. Gene expression levels of RAGE, HMGB1, TLR2, TLR4, and NF-kB were significantly greater in the CHLs and IGHLs from the FS group than in those from the RCT group. Immunoreactivities of RAGE and CML were stronger in the CHLs and IGHLs from the FS group than in those from the RCT group. Pentosidine was weakly immunostained in the CHLs and IGHLs from the FS group. CML using high-performance liquid chromatography was significantly greater in the CHLs and IGHLs from the FS group than in those from the RCT group. AGEs and HMGB1 might play important roles in the pathogenesis of FS by binding to RAGE and activating NF-kB signaling pathways. Suppression of these pathways could be a treatment option for FS.
Sections du résumé
BACKGROUND
BACKGROUND
The etiology of frozen shoulder (FS) remains uncertain. Advanced glycation end-products (AGEs) cause the cross-linking and stabilization of collagen and are increased in FS. The purpose of this study was to elucidate the pathogenesis of FS by evaluating the receptor of AGE (RAGE)-dependent pathways.
METHODS
METHODS
Tissue samples of the coracohumeral ligament (CHL) and anterior inferior glenohumeral ligament (IGHL) were collected from 33 patients with FS, with severe stiffness, and 25 with rotator cuff tears (RCTs) as controls. Gene expression levels of RAGE, high-mobility group box 1 (HMGB1), Toll-like receptor 2 (TLR2), TLR4, nuclear factor-kappa B (NF-kB), and cytokines were evaluated using a quantitative real-time polymerase chain reaction. The immunoreactivities of carboxymethyllysine (CML), pentosidine, and RAGE were also evaluated. CML and pentosidine were further evaluated using high-performance liquid chromatography.
RESULTS
RESULTS
Gene expression levels of RAGE, HMGB1, TLR2, TLR4, and NF-kB were significantly greater in the CHLs and IGHLs from the FS group than in those from the RCT group. Immunoreactivities of RAGE and CML were stronger in the CHLs and IGHLs from the FS group than in those from the RCT group. Pentosidine was weakly immunostained in the CHLs and IGHLs from the FS group. CML using high-performance liquid chromatography was significantly greater in the CHLs and IGHLs from the FS group than in those from the RCT group.
CONCLUSIONS
CONCLUSIONS
AGEs and HMGB1 might play important roles in the pathogenesis of FS by binding to RAGE and activating NF-kB signaling pathways. Suppression of these pathways could be a treatment option for FS.
Identifiants
pubmed: 32279986
pii: S1058-2746(20)30113-0
doi: 10.1016/j.jse.2020.01.076
pii:
doi:
Substances chimiques
HMGB1 Protein
0
NF-kappa B
0
Receptor for Advanced Glycation End Products
0
TLR2 protein, human
0
TLR4 protein, human
0
Toll-Like Receptor 2
0
Toll-Like Receptor 4
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
1884-1891Informations de copyright
Copyright © 2020 Journal of Shoulder and Elbow Surgery Board of Trustees. Published by Elsevier Inc. All rights reserved.