Chondroprotective effects of platelet lysate towards monoiodoacetate-induced arthritis by suppression of TNF-α-induced activation of NF-κB pathway in chondrocytes

Publication type:
Journal article
Metadata:
Autoren
  • Li Yan
  • Li Zhou
  • Danting Xie
  • Wenxi Du
  • Fangming Chen
  • Qiang Yuan
  • Peijian Tong
  • Letian Shan
  • Thomas Efferth
Autoren-URL
https://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=fis-test-1&SrcAuth=WosAPI&KeyUT=WOS:000468332900019&DestLinkType=FullRecord&DestApp=WOS_CPL
DOI
10.18632/aging.101952
Externe Identifier
  • Clarivate Analytics Document Solution ID: HY7RE
  • PubMed Identifier: 31089001
ISSN
1945-4589
Ausgabe der Veröffentlichung
9
Zeitschrift
AGING-US
Schlüsselwörter
  • platelet lysate
  • growth factor
  • osteoarthritis
  • TNF-alpha
  • NF-kappa B
Paginierung
2797 - 2811
Datum der Veröffentlichung
2019
Status
Published
Titel
Chondroprotective effects of platelet lysate towards monoiodoacetate-induced arthritis by suppression of TNF-α-induced activation of NF-κB pathway in chondrocytes
Sub types
  • Article
Ausgabe der Zeitschrift
11

Data source: Web of Science (Lite)

Other metadata sources:
Autoren
  • Li Yan
  • Li Zhou
  • Danting Xie
  • Wenxi Du
  • Fangming Chen
  • Qiang Yuan
  • Peijian Tong
  • Letian Shan
  • Thomas Efferth
DOI
10.18632/aging.101952
eISSN
1945-4589
Ausgabe der Veröffentlichung
9
Zeitschrift
Aging
Sprache
en
Online publication date
2019
Paginierung
2797 - 2811
Datum der Veröffentlichung
2019
Status
Published
Herausgeber
Impact Journals, LLC
Herausgeber URL
http://dx.doi.org/10.18632/aging.101952
Datum der Datenerfassung
2020
Titel
Chondroprotective effects of platelet lysate towards monoiodoacetate-induced arthritis by suppression of TNF-α-induced activation of NF-ĸB pathway in chondrocytes
Ausgabe der Zeitschrift
11

Data source: Crossref

Abstract
Platelet lysate (PL) contains a cocktail of growth factors that actively participates in cartilage repair. This study was designed to determine the effect and mechanism of PL on osteoarthritis (OA). An arthritis model was established to mimic human OA by intra-articular injection of monoiodoacetate (MIA) to Sprague Dawley (SD) rats. The model was weekly treated with PL by intra-articular injection. Thermal withdrawal latency, mechanical withdrawal threshold, and treadmill gait were tested for pain behavior observation. Histopathological and immunohistochemical analyses were conducted for evaluating cartilage degradation. Real time PCRs and Western blots were conducted to elucidate the mechanism of PL on primary chondrocytes. Results showed that, <i>in vivo</i>, PL significantly attenuated pain symptoms and exerted chondrocyte-protective and extracellular matrix (ECM)-modifying effect on the arthritic cartilage in a dose-dependent manner. The <i>in situ</i> expressions of type II Collagen (Col2) and matrix metalloproteinase 13 (Mmp13) in the arthritic cartilage was abnormal and was restored by PL. <i>In vitro</i>, PL significantly restored tumor necrosis factor α (TNF-α)-suppressed anabolic gene expression (<i>Col2</i> and <i>aggrecan</i>) and TNF-α-increased catabolic gene expression (<i>Col10</i>, <i>Mmp13</i>, <i>Adamts5</i>, and <i>Adamts9</i>) in chondrocytes. The effects were mediated by TNF-α downstream signaling, including inhibition of NF-κB and c-Jun activities. This study provides certain knowledge of anti-OA effect and TNF signaling-related mechanism of PL, placing it as a promising and alternative option for OA therapy in the future.
Addresses
  • The First Affiliated Hospital, Zhejiang Chinese Medical University, Hangzhou, China.
Autoren
  • Li Yan
  • Li Zhou
  • Danting Xie
  • Wenxi Du
  • Fangming Chen
  • Qiang Yuan
  • Peijian Tong
  • Letian Shan
  • Thomas Efferth
DOI
10.18632/aging.101952
eISSN
1945-4589
Externe Identifier
  • PubMed Identifier: 31089001
  • PubMed Central ID: PMC6535074
Open access
true
ISSN
1945-4589
Ausgabe der Veröffentlichung
9
Zeitschrift
Aging
Schlüsselwörter
  • Blood Platelets
  • Chondrocytes
  • Animals
  • Humans
  • Rats
  • Rats, Sprague-Dawley
  • Arthritis
  • Osteoarthritis
  • Pain
  • Iodoacetic Acid
  • Tumor Necrosis Factor-alpha
  • NF-kappa B
  • Analgesics
  • Random Allocation
  • Cell Survival
  • Gene Expression Regulation
  • Male
Sprache
eng
Medium
Print
Open access status
Open Access
Paginierung
2797 - 2811
Datum der Veröffentlichung
2019
Status
Published
Publisher licence
CC BY
Datum der Datenerfassung
2019
Titel
Chondroprotective effects of platelet lysate towards monoiodoacetate-induced arthritis by suppression of TNF-α-induced activation of NF-ĸB pathway in chondrocytes.
Sub types
  • Research Support, Non-U.S. Gov't
  • research-article
  • Journal Article
Ausgabe der Zeitschrift
11

Files

https://europepmc.org/articles/PMC6535074?pdf=render

Data source: Europe PubMed Central

Abstract
Platelet lysate (PL) contains a cocktail of growth factors that actively participates in cartilage repair. This study was designed to determine the effect and mechanism of PL on osteoarthritis (OA). An arthritis model was established to mimic human OA by intra-articular injection of monoiodoacetate (MIA) to Sprague Dawley (SD) rats. The model was weekly treated with PL by intra-articular injection. Thermal withdrawal latency, mechanical withdrawal threshold, and treadmill gait were tested for pain behavior observation. Histopathological and immunohistochemical analyses were conducted for evaluating cartilage degradation. Real time PCRs and Western blots were conducted to elucidate the mechanism of PL on primary chondrocytes. Results showed that, in vivo, PL significantly attenuated pain symptoms and exerted chondrocyte-protective and extracellular matrix (ECM)-modifying effect on the arthritic cartilage in a dose-dependent manner. The in situ expressions of type II Collagen (Col2) and matrix metalloproteinase 13 (Mmp13) in the arthritic cartilage was abnormal and was restored by PL. In vitro, PL significantly restored tumor necrosis factor α (TNF-α)-suppressed anabolic gene expression (Col2 and aggrecan) and TNF-α-increased catabolic gene expression (Col10, Mmp13, Adamts5, and Adamts9) in chondrocytes. The effects were mediated by TNF-α downstream signaling, including inhibition of NF-κB and c-Jun activities. This study provides certain knowledge of anti-OA effect and TNF signaling-related mechanism of PL, placing it as a promising and alternative option for OA therapy in the future.
Date of acceptance
2019
Autoren
  • Li Yan
  • Li Zhou
  • Danting Xie
  • Wenxi Du
  • Fangming Chen
  • Qiang Yuan
  • Peijian Tong
  • Letian Shan
  • Thomas Efferth
Autoren-URL
https://www.ncbi.nlm.nih.gov/pubmed/31089001
DOI
10.18632/aging.101952
eISSN
1945-4589
Externe Identifier
  • PubMed Central ID: PMC6535074
Ausgabe der Veröffentlichung
9
Zeitschrift
Aging (Albany NY)
Schlüsselwörter
  • NF-κB
  • TNF-α
  • growth factor
  • osteoarthritis
  • platelet lysate
  • Analgesics
  • Animals
  • Arthritis
  • Blood Platelets
  • Cell Survival
  • Chondrocytes
  • Gene Expression Regulation
  • Humans
  • Iodoacetic Acid
  • Male
  • NF-kappa B
  • Osteoarthritis
  • Pain
  • Random Allocation
  • Rats
  • Rats, Sprague-Dawley
  • Tumor Necrosis Factor-alpha
Sprache
eng
Country
United States
Paginierung
2797 - 2811
PII
101952
Datum der Veröffentlichung
2019
Status
Published
Datum, an dem der Datensatz öffentlich gemacht wurde
2020
Titel
Chondroprotective effects of platelet lysate towards monoiodoacetate-induced arthritis by suppression of TNF-α-induced activation of NF-ĸB pathway in chondrocytes.
Sub types
  • Journal Article
  • Research Support, Non-U.S. Gov't
Ausgabe der Zeitschrift
11

Data source: PubMed

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