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Culture-expanded allogenic adipose tissue-derived stem cells attenuate cartilage degeneration in an experimental rat osteoarthritis model.

Abstract Mesenchymal stem cell (MSC)-based cell therapy is a promising avenue for osteoarthritis (OA) treatment. In the present study, we evaluated the efficacy of intra-articular injections of culture-expanded allogenic adipose tissue-derived stem cells (ADSCs) for the treatment of anterior cruciate ligament transection (ACLT) induced rat OA model. The paracrine effects of major histocompatibility complex (MHC)-unmatched ADSCs on chondrocytes were investigated in vitro. Rats were divided into an OA group that underwent ACLT surgery and a sham-operated group that did not undergo ACLT surgery. Four weeks after surgery mild OA was induced in the OA group. Subsequently, the OA rats were randomly divided into ADSC and control groups. A single dose of 1 × 106 ADSCs suspended in 60 μL phosphate-buffered saline (PBS) was intra-articularly injected into the rats of the ADSC group. The control group received only 60 μL PBS. OA progression was evaluated macroscopically and histologically at 8 and 12 weeks after surgery. ADSC treatment did not cause any adverse local or systemic reactions. The degeneration of articular cartilage was significantly weaker in the ADSC group compared to that in the control group at both 8 and 12 weeks. Chondrocytes were co-cultured with MHC-unmatched ADSCs in trans-wells to assess the paracrine effects of ADSCs on chondrocytes. Co-culture with ADSCs counteracted the IL-1β-induced mRNA upregulation of the extracellular matrix-degrading enzymes MMP-3 and MMP-13 and the pro-inflammatory cytokines TNF-α and IL-6 in chondrocytes. Importantly, ADSCs increased the expression of the anti-inflammatory cytokine IL-10 in chondrocytes. The results of this study indicated that the intra-articular injection of culture-expanded allogenic ADSCs attenuated cartilage degeneration in an experimental rat OA model without inducing any adverse reactions. MHC-unmatched ADSCs protected chondrocytes from inflammatory factor-induced damage. The paracrine effects of ADSCs on OA chondrocytes are at least part of the mechanism by which ADSCs exert their therapeutic activity.
PMID
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The paracrine effect of adipose-derived stem cells inhibits osteoarthritis progression.

Authors

Mayor MeshTerms
Keywords
Journal Title plos one
Publication Year Start




PMID- 28419155
OWN - NLM
STAT- In-Process
DA  - 20170418
LR  - 20170418
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 12
IP  - 4
DP  - 2017
TI  - Culture-expanded allogenic adipose tissue-derived stem cells attenuate cartilage 
      degeneration in an experimental rat osteoarthritis model.
PG  - e0176107
LID - 10.1371/journal.pone.0176107 [doi]
AB  - Mesenchymal stem cell (MSC)-based cell therapy is a promising avenue for
      osteoarthritis (OA) treatment. In the present study, we evaluated the efficacy of
      intra-articular injections of culture-expanded allogenic adipose tissue-derived
      stem cells (ADSCs) for the treatment of anterior cruciate ligament transection
      (ACLT) induced rat OA model. The paracrine effects of major histocompatibility
      complex (MHC)-unmatched ADSCs on chondrocytes were investigated in vitro. Rats
      were divided into an OA group that underwent ACLT surgery and a sham-operated
      group that did not undergo ACLT surgery. Four weeks after surgery mild OA was
      induced in the OA group. Subsequently, the OA rats were randomly divided into
      ADSC and control groups. A single dose of 1 x 106 ADSCs suspended in 60 muL
      phosphate-buffered saline (PBS) was intra-articularly injected into the rats of
      the ADSC group. The control group received only 60 muL PBS. OA progression was
      evaluated macroscopically and histologically at 8 and 12 weeks after surgery.
      ADSC treatment did not cause any adverse local or systemic reactions. The
      degeneration of articular cartilage was significantly weaker in the ADSC group
      compared to that in the control group at both 8 and 12 weeks. Chondrocytes were
      co-cultured with MHC-unmatched ADSCs in trans-wells to assess the paracrine
      effects of ADSCs on chondrocytes. Co-culture with ADSCs counteracted the
      IL-1beta-induced mRNA upregulation of the extracellular matrix-degrading enzymes 
      MMP-3 and MMP-13 and the pro-inflammatory cytokines TNF-alpha and IL-6 in
      chondrocytes. Importantly, ADSCs increased the expression of the
      anti-inflammatory cytokine IL-10 in chondrocytes. The results of this study
      indicated that the intra-articular injection of culture-expanded allogenic ADSCs 
      attenuated cartilage degeneration in an experimental rat OA model without
      inducing any adverse reactions. MHC-unmatched ADSCs protected chondrocytes from
      inflammatory factor-induced damage. The paracrine effects of ADSCs on OA
      chondrocytes are at least part of the mechanism by which ADSCs exert their
      therapeutic activity.
FAU - Mei, Li
AU  - Mei L
AD  - School of Pharmaceutical Sciences, Shandong University, Jinan, Shandong Province,
      People's Republic of China.
AD  - Post-doctoral Scientific Research Workstation, Shandong Academy of Pharmaceutical
      Science, Jinan, Shandong Province, People's Republic of China.
FAU - Shen, Bojiang
AU  - Shen B
AD  - Department of Orthopedic Research, Orthopedic Research Institute, St George
      Hospital University of New South Wales, Sydney, Australia.
FAU - Ling, Peixue
AU  - Ling P
AUID- ORCID: http://orcid.org/0000-0002-0382-1571
AD  - School of Pharmaceutical Sciences, Shandong University, Jinan, Shandong Province,
      People's Republic of China.
AD  - Post-doctoral Scientific Research Workstation, Shandong Academy of Pharmaceutical
      Science, Jinan, Shandong Province, People's Republic of China.
FAU - Liu, Shaoying
AU  - Liu S
AD  - Post-doctoral Scientific Research Workstation, Shandong Academy of Pharmaceutical
      Science, Jinan, Shandong Province, People's Republic of China.
FAU - Xue, Jiajun
AU  - Xue J
AD  - Post-doctoral Scientific Research Workstation, Shandong Academy of Pharmaceutical
      Science, Jinan, Shandong Province, People's Republic of China.
FAU - Liu, Fuyan
AU  - Liu F
AD  - School of Pharmaceutical Sciences, Shandong University, Jinan, Shandong Province,
      People's Republic of China.
AD  - Post-doctoral Scientific Research Workstation, Shandong Academy of Pharmaceutical
      Science, Jinan, Shandong Province, People's Republic of China.
FAU - Shao, Huarong
AU  - Shao H
AD  - Post-doctoral Scientific Research Workstation, Shandong Academy of Pharmaceutical
      Science, Jinan, Shandong Province, People's Republic of China.
FAU - Chen, Jianying
AU  - Chen J
AD  - Post-doctoral Scientific Research Workstation, Shandong Academy of Pharmaceutical
      Science, Jinan, Shandong Province, People's Republic of China.
FAU - Ma, Aibin
AU  - Ma A
AD  - School of Pharmaceutical Sciences, Shandong University, Jinan, Shandong Province,
      People's Republic of China.
AD  - Post-doctoral Scientific Research Workstation, Shandong Academy of Pharmaceutical
      Science, Jinan, Shandong Province, People's Republic of China.
FAU - Liu, Xia
AU  - Liu X
AD  - Post-doctoral Scientific Research Workstation, Shandong Academy of Pharmaceutical
      Science, Jinan, Shandong Province, People's Republic of China.
LA  - eng
PT  - Journal Article
DEP - 20170418
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
EDAT- 2017/04/19 06:00
MHDA- 2017/04/19 06:00
CRDT- 2017/04/19 06:00
PHST- 2016/12/13 [received]
PHST- 2017/04/05 [accepted]
AID - 10.1371/journal.pone.0176107 [doi]
AID - PONE-D-16-49165 [pii]
PST - epublish
SO  - PLoS One. 2017 Apr 18;12(4):e0176107. doi: 10.1371/journal.pone.0176107.
      eCollection 2017.

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