Platelet-Rich Plasma Attenuates 30-kDa Fibronectin Fragment-Induced Chemokine and Matrix Metalloproteinase Expression by Meniscocytes and Articular Chondrocytes

Chih Chien Wang, Chian Her Lee, Yi Jen Peng, Donald M. Salter, Herng Sheng Lee

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

Background: Proteolytic fragments of fibronectin have catabolic effects on cartilage and menisci. Platelet-rich plasma (PRP) is increasingly being used to treat a range of joint conditions, but it is unknown whether PRP influences fibronectin fragment (FN-f) procatabolic activity. Hypotheses: The procatabolic activity of FN-f on meniscocytes and articular chondrocytes is attenuated by cotreatment with PRP. Study Design: Controlled laboratory study. Methods: Human meniscocytes were treated with FN-f (30 kDa) with or without PRP coincubation, and gene expression was analyzed by complementary DNA microarray analysis. Validation of altered expression of known and novel chemokine and protease genes was undertaken by real-time polymerase chain reaction (RT-PCR) in articular chondrocytes and meniscocytes. Chemokine release was assayed by enzyme-linked immunosorbent assay, and intracellular pathway signaling was evaluated by Western immunoblotting. Results: Microarray analysis and RT-PCR showed increased expression of matrix metalloproteinase (MMP)1, MMP2, MMP3, MMP9, MMP13, interleukin (IL)-6, IL-8 (CXCL8), CCL5, CCL20, and CXCL10 chemokines in meniscocytes after treatment with FN-f. Upregulation of these genes was significantly attenuated by PRP. Similar results were seen with articular chondrocytes, although no changes in MMP2 or MMP9 levels were identified. PRP-induced suppression of gene expression was associated with activation of Akt and p44/p42. Conclusion: PRP treatment attenuates the 30-kDa FN-f-induced expression of a range of proinflammatory chemokines and MMPs, including IL-8, IL-6, CCL20, CCL5, CXCL10, MMP1, MMP3, and MMP13, by both meniscocytes and articular chondrocytes. Clinical Relevance: These observations provide support for the use and further trials of PRP in management of cartilage and meniscal injuries.

Original languageEnglish
Pages (from-to)2481-2489
Number of pages9
JournalAmerican Journal of Sports Medicine
Volume43
Issue number10
DOIs
Publication statusPublished - Oct 1 2015

Fingerprint

Platelet-Rich Plasma
Chondrocytes
Matrix Metalloproteinases
Fibronectins
Chemokines
Joints
Interleukin-8
Microarray Analysis
Cartilage
Real-Time Polymerase Chain Reaction
Interleukin-6
Gene Expression
Matrix Metalloproteinase 1
Oligonucleotide Array Sequence Analysis
Genes
Peptide Hydrolases
Up-Regulation
Complementary DNA
Western Blotting
Enzyme-Linked Immunosorbent Assay

Keywords

  • chemokine
  • chondrocyte
  • fibronectin fragment
  • matrix metalloproteinase
  • platelet-rich plasma

ASJC Scopus subject areas

  • Orthopedics and Sports Medicine
  • Physical Therapy, Sports Therapy and Rehabilitation

Cite this

Platelet-Rich Plasma Attenuates 30-kDa Fibronectin Fragment-Induced Chemokine and Matrix Metalloproteinase Expression by Meniscocytes and Articular Chondrocytes. / Wang, Chih Chien; Lee, Chian Her; Peng, Yi Jen; Salter, Donald M.; Lee, Herng Sheng.

In: American Journal of Sports Medicine, Vol. 43, No. 10, 01.10.2015, p. 2481-2489.

Research output: Contribution to journalArticle

@article{872cc483f6304c50909e20c3597b08f8,
title = "Platelet-Rich Plasma Attenuates 30-kDa Fibronectin Fragment-Induced Chemokine and Matrix Metalloproteinase Expression by Meniscocytes and Articular Chondrocytes",
abstract = "Background: Proteolytic fragments of fibronectin have catabolic effects on cartilage and menisci. Platelet-rich plasma (PRP) is increasingly being used to treat a range of joint conditions, but it is unknown whether PRP influences fibronectin fragment (FN-f) procatabolic activity. Hypotheses: The procatabolic activity of FN-f on meniscocytes and articular chondrocytes is attenuated by cotreatment with PRP. Study Design: Controlled laboratory study. Methods: Human meniscocytes were treated with FN-f (30 kDa) with or without PRP coincubation, and gene expression was analyzed by complementary DNA microarray analysis. Validation of altered expression of known and novel chemokine and protease genes was undertaken by real-time polymerase chain reaction (RT-PCR) in articular chondrocytes and meniscocytes. Chemokine release was assayed by enzyme-linked immunosorbent assay, and intracellular pathway signaling was evaluated by Western immunoblotting. Results: Microarray analysis and RT-PCR showed increased expression of matrix metalloproteinase (MMP)1, MMP2, MMP3, MMP9, MMP13, interleukin (IL)-6, IL-8 (CXCL8), CCL5, CCL20, and CXCL10 chemokines in meniscocytes after treatment with FN-f. Upregulation of these genes was significantly attenuated by PRP. Similar results were seen with articular chondrocytes, although no changes in MMP2 or MMP9 levels were identified. PRP-induced suppression of gene expression was associated with activation of Akt and p44/p42. Conclusion: PRP treatment attenuates the 30-kDa FN-f-induced expression of a range of proinflammatory chemokines and MMPs, including IL-8, IL-6, CCL20, CCL5, CXCL10, MMP1, MMP3, and MMP13, by both meniscocytes and articular chondrocytes. Clinical Relevance: These observations provide support for the use and further trials of PRP in management of cartilage and meniscal injuries.",
keywords = "chemokine, chondrocyte, fibronectin fragment, matrix metalloproteinase, platelet-rich plasma",
author = "Wang, {Chih Chien} and Lee, {Chian Her} and Peng, {Yi Jen} and Salter, {Donald M.} and Lee, {Herng Sheng}",
year = "2015",
month = "10",
day = "1",
doi = "10.1177/0363546515597489",
language = "English",
volume = "43",
pages = "2481--2489",
journal = "American Journal of Sports Medicine",
issn = "0363-5465",
publisher = "SAGE Publications Inc.",
number = "10",

}

TY - JOUR

T1 - Platelet-Rich Plasma Attenuates 30-kDa Fibronectin Fragment-Induced Chemokine and Matrix Metalloproteinase Expression by Meniscocytes and Articular Chondrocytes

AU - Wang, Chih Chien

AU - Lee, Chian Her

AU - Peng, Yi Jen

AU - Salter, Donald M.

AU - Lee, Herng Sheng

PY - 2015/10/1

Y1 - 2015/10/1

N2 - Background: Proteolytic fragments of fibronectin have catabolic effects on cartilage and menisci. Platelet-rich plasma (PRP) is increasingly being used to treat a range of joint conditions, but it is unknown whether PRP influences fibronectin fragment (FN-f) procatabolic activity. Hypotheses: The procatabolic activity of FN-f on meniscocytes and articular chondrocytes is attenuated by cotreatment with PRP. Study Design: Controlled laboratory study. Methods: Human meniscocytes were treated with FN-f (30 kDa) with or without PRP coincubation, and gene expression was analyzed by complementary DNA microarray analysis. Validation of altered expression of known and novel chemokine and protease genes was undertaken by real-time polymerase chain reaction (RT-PCR) in articular chondrocytes and meniscocytes. Chemokine release was assayed by enzyme-linked immunosorbent assay, and intracellular pathway signaling was evaluated by Western immunoblotting. Results: Microarray analysis and RT-PCR showed increased expression of matrix metalloproteinase (MMP)1, MMP2, MMP3, MMP9, MMP13, interleukin (IL)-6, IL-8 (CXCL8), CCL5, CCL20, and CXCL10 chemokines in meniscocytes after treatment with FN-f. Upregulation of these genes was significantly attenuated by PRP. Similar results were seen with articular chondrocytes, although no changes in MMP2 or MMP9 levels were identified. PRP-induced suppression of gene expression was associated with activation of Akt and p44/p42. Conclusion: PRP treatment attenuates the 30-kDa FN-f-induced expression of a range of proinflammatory chemokines and MMPs, including IL-8, IL-6, CCL20, CCL5, CXCL10, MMP1, MMP3, and MMP13, by both meniscocytes and articular chondrocytes. Clinical Relevance: These observations provide support for the use and further trials of PRP in management of cartilage and meniscal injuries.

AB - Background: Proteolytic fragments of fibronectin have catabolic effects on cartilage and menisci. Platelet-rich plasma (PRP) is increasingly being used to treat a range of joint conditions, but it is unknown whether PRP influences fibronectin fragment (FN-f) procatabolic activity. Hypotheses: The procatabolic activity of FN-f on meniscocytes and articular chondrocytes is attenuated by cotreatment with PRP. Study Design: Controlled laboratory study. Methods: Human meniscocytes were treated with FN-f (30 kDa) with or without PRP coincubation, and gene expression was analyzed by complementary DNA microarray analysis. Validation of altered expression of known and novel chemokine and protease genes was undertaken by real-time polymerase chain reaction (RT-PCR) in articular chondrocytes and meniscocytes. Chemokine release was assayed by enzyme-linked immunosorbent assay, and intracellular pathway signaling was evaluated by Western immunoblotting. Results: Microarray analysis and RT-PCR showed increased expression of matrix metalloproteinase (MMP)1, MMP2, MMP3, MMP9, MMP13, interleukin (IL)-6, IL-8 (CXCL8), CCL5, CCL20, and CXCL10 chemokines in meniscocytes after treatment with FN-f. Upregulation of these genes was significantly attenuated by PRP. Similar results were seen with articular chondrocytes, although no changes in MMP2 or MMP9 levels were identified. PRP-induced suppression of gene expression was associated with activation of Akt and p44/p42. Conclusion: PRP treatment attenuates the 30-kDa FN-f-induced expression of a range of proinflammatory chemokines and MMPs, including IL-8, IL-6, CCL20, CCL5, CXCL10, MMP1, MMP3, and MMP13, by both meniscocytes and articular chondrocytes. Clinical Relevance: These observations provide support for the use and further trials of PRP in management of cartilage and meniscal injuries.

KW - chemokine

KW - chondrocyte

KW - fibronectin fragment

KW - matrix metalloproteinase

KW - platelet-rich plasma

UR - http://www.scopus.com/inward/record.url?scp=84942936509&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84942936509&partnerID=8YFLogxK

U2 - 10.1177/0363546515597489

DO - 10.1177/0363546515597489

M3 - Article

VL - 43

SP - 2481

EP - 2489

JO - American Journal of Sports Medicine

JF - American Journal of Sports Medicine

SN - 0363-5465

IS - 10

ER -