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Transforming growth factor β1 enhances heme oxygenase 1 expression in human synovial fibroblasts by inhibiting microRNA 519b synthesis.

Abstract Osteoarthritis (OA) is manifested by synovial inflammation and cartilage destruction that is directly linked to synovitis, joint swelling and pain. In the light of the role of synovium in the pathogenesis and the symptoms of OA, synovium-targeted therapy is a promising strategy to mitigate the symptoms and progression of OA. Transforming growth factor beta 1 (TGF-β1), a secreted homodimeric protein, possesses unique and potent anti-inflammatory and immune-regulatory properties in many cell types. Heme oxygenase 1 (HO-1) is an inducible anti-inflammatory and stress responsive enzyme that has been proven to prevent injuries caused by many diseases. Despite the similar anti-inflammatory profile and their involvement in the pathogenesis of arthritic diseases, no studies have as yet explored the possibility of any association between the expression of TGF-β1 and HO-1.
PMID
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Mayor MeshTerms
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Journal Title plos one
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PMID- 28423042
OWN - NLM
STAT- In-Process
DA  - 20170419
LR  - 20170419
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 12
IP  - 4
DP  - 2017
TI  - Transforming growth factor beta1 enhances heme oxygenase 1 expression in human
      synovial fibroblasts by inhibiting microRNA 519b synthesis.
PG  - e0176052
LID - 10.1371/journal.pone.0176052 [doi]
AB  - BACKGROUND: Osteoarthritis (OA) is manifested by synovial inflammation and
      cartilage destruction that is directly linked to synovitis, joint swelling and
      pain. In the light of the role of synovium in the pathogenesis and the symptoms
      of OA, synovium-targeted therapy is a promising strategy to mitigate the symptoms
      and progression of OA. Transforming growth factor beta 1 (TGF-beta1), a secreted 
      homodimeric protein, possesses unique and potent anti-inflammatory and
      immune-regulatory properties in many cell types. Heme oxygenase 1 (HO-1) is an
      inducible anti-inflammatory and stress responsive enzyme that has been proven to 
      prevent injuries caused by many diseases. Despite the similar anti-inflammatory
      profile and their involvement in the pathogenesis of arthritic diseases, no
      studies have as yet explored the possibility of any association between the
      expression of TGF-beta1 and HO-1. METHODOLOGY/PRINCIPAL FINDINGS:
      TGF-beta1-induced HO-1 expression was examined by HO-1 promoter assay, qPCR, and 
      Western blotting. The siRNAs and enzyme inhibitors were utilized to determine the
      intermediate involved in the signal transduction pathway. We showed that
      TGF-beta1 stimulated the synthesis of HO-1 in a concentration- and time-dependent
      manner, which can be mitigated by blockade of the phospholipase
      (PLC)gamma/protein kinase C alpha (PKC)alpha pathway. We also showed that the
      expression of miRNA-519b, which blocks HO-1 transcription, is inhibited by
      TGF-beta1, and the suppression of miRNA 519b could be reversed via blockade of
      the PLCgamma/PKCalpha pathway. CONCLUSIONS/SIGNIFICANCE: TGF-beta1 stimulated the
      expression of HO-1 via activating the PLCgamma/PKCalpha pathway and suppressing
      the downstream expression of miRNA-519b. These results may shed light on the
      pathogenesis and treatment of OA.
FAU - Kuo, Shu-Jui
AU  - Kuo SJ
AD  - Graduate Institute of Clinical Medical Science, China Medical University,
      Taichung, Taiwan.
AD  - Department of Orthopedic Surgery, China Medical University Hospital, Taichung,
      Taiwan.
FAU - Yang, Wei-Hung
AU  - Yang WH
AD  - Department of Orthopedic Surgery, Taichung Hospital, Ministry of Health and
      Welfare, Taichung, Taiwan.
AD  - School of Chinese Medicine, China Medical University, Taichung, Taiwan.
AD  - Department of Nursing, National Taichung University of Science and Technology,
      Taichung, Taiwan.
AD  - Graduate Institute of Biotechnology, National Chung Hsing University, Taichung,
      Taiwan.
FAU - Liu, Shan-Chi
AU  - Liu SC
AD  - Graduate Institute of Basic Medical Science, China Medical University, Taichung, 
      Taiwan.
FAU - Tsai, Chun-Hao
AU  - Tsai CH
AD  - Graduate Institute of Clinical Medical Science, China Medical University,
      Taichung, Taiwan.
AD  - Department of Orthopedic Surgery, China Medical University Hospital, Taichung,
      Taiwan.
FAU - Hsu, Horng-Chaung
AU  - Hsu HC
AD  - Graduate Institute of Clinical Medical Science, China Medical University,
      Taichung, Taiwan.
AD  - Department of Orthopedic Surgery, China Medical University Hospital, Taichung,
      Taiwan.
FAU - Tang, Chih-Hsin
AU  - Tang CH
AUID- ORCID: http://orcid.org/0000-0002-7113-8352
AD  - Graduate Institute of Basic Medical Science, China Medical University, Taichung, 
      Taiwan.
AD  - Department of Pharmacology, School of Medicine, China Medical University,
      Taichung, Taiwan.
AD  - Department of Biotechnology, College of Health Science, Asia University,
      Taichung, Taiwan.
LA  - eng
PT  - Journal Article
DEP - 20170419
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
EDAT- 2017/04/20 06:00
MHDA- 2017/04/20 06:00
CRDT- 2017/04/20 06:00
PHST- 2017/01/13 [received]
PHST- 2017/04/04 [accepted]
AID - 10.1371/journal.pone.0176052 [doi]
AID - PONE-D-17-01650 [pii]
PST - epublish
SO  - PLoS One. 2017 Apr 19;12(4):e0176052. doi: 10.1371/journal.pone.0176052.
      eCollection 2017.

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