PMID- 25926140
OWN - NLM
STAT- MEDLINE
DCOM- 20160308
LR  - 20150526
IS  - 1745-7270 (Electronic)
IS  - 1672-9145 (Linking)
VI  - 47
IP  - 6
DP  - 2015 Jun
TI  - Poly(ADP-ribose) polymerase 1 inhibition prevents interleukin-1beta-induced 
      inflammation in human osteoarthritic chondrocytes.
PG  - 422-30
LID - 10.1093/abbs/gmv033 [doi]
AB  - Osteoarthritis (OA) is an age-related joint disease that is characterized by the 
      degeneration of articular chondrocytes. Nuclear enzyme poly(ADP-ribose) 
      polymerase 1 (PARP-1) is associated with inflammation response. We investigated 
      the role of PARP-1 in interleukin-1beta (IL-1beta)-stimulated human articular 
      chondrocytes and its underlying mechanism. Cell viability and apoptosis were 
      evaluated by using 3-(4,5)-dimethylthiahiazo(-z-y1)-3,5-di-phenytetrazoliumromide 
      assay and flow cytometry, respectively. Tumor necrosis factor-alpha (TNF-alpha) level was 
      measured by enzyme-linked immunosorbent assay. The mRNA and protein expression 
      levels of PARP-1, IL-1 receptor (IL-1R), inducible nitric oxide synthase (iNOS), 
      matrix metalloproteinases (MMPs), and tissue inhibitor of metalloproteinases-1 
      (TIMP-1) were determined by real-time reverse transcriptase-polymerase chain 
      reaction and western blot analysis, respectively. The expression and 
      phosphorylation of NF-small ka, CyrillicB p65 were measured by western blot analysis. Results 
      showed that stimulation of chondrocytes with IL-1beta caused a significant 
      up-regulation of PARP-1 and IL-1R, resulting in NF-small ka, CyrillicB p65 nuclear translocation 
      and phosphorylation associated with an increase of TNF-alpha secretion and iNOS 
      expression. PARP-1 was inhibited by siRNA transfection. Results showed that 
      PARP-1 inhibition suppressed IL-1beta-induced reduction of cell viability and 
      up-regulation of cell apoptosis, with a reduced IL-1R expression. PARP-1 
      inhibition also effectively reversed IL-1beta-induced inflammatory response through 
      inhibiting the IL-1R/NF-small ka, CyrillicB pathway. These data suggested that PARP-1 inhibition 
      prevents IL-1beta-induced inflammation response at least partly by inhibiting the 
      IL-1R/NF-small ka, CyrillicB signaling pathway in human articular chondrocytes. Moreover, PARP-1 
      inhibition reduced MMPs expression and increased TIMP-1 expression, suggesting 
      that PARP-1 inhibition could suppress cartilage destruction by modulating the 
      balance between MMPs and TIMP-1. Inhibition of PARP-1 might be useful in the 
      treatment of OA.
CI  - (c) The Author 2015. Published by ABBS Editorial Office in association with Oxford 
      University Press on behalf of the Institute of Biochemistry and Cell Biology, 
      Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences.
FAU - Sun, Yujie
AU  - Sun Y
AD  - Orthopedics Department, Yantai Yuhuangding Hospital, Affiliated by Qingdao 
      University Medical College, Yantai 264000, China.
FAU - Zhou, Lugang
AU  - Zhou L
AD  - Orthopedics Department, Yantai Yuhuangding Hospital, Affiliated by Qingdao 
      University Medical College, Yantai 264000, China.
FAU - Lv, Dongmei
AU  - Lv D
AD  - Orthopedics Department, Yantai Yuhuangding Hospital, Affiliated by Qingdao 
      University Medical College, Yantai 264000, China.
FAU - Liu, Hongzhi
AU  - Liu H
AD  - Orthopedics Department, Yantai Yuhuangding Hospital, Affiliated by Qingdao 
      University Medical College, Yantai 264000, China.
FAU - He, Tian
AU  - He T
AD  - Orthopedics Department, Yantai Yuhuangding Hospital, Affiliated by Qingdao 
      University Medical College, Yantai 264000, China.
FAU - Wang, Xin
AU  - Wang X
AD  - Orthopedics Department, Yantai Yuhuangding Hospital, Affiliated by Qingdao 
      University Medical College, Yantai 264000, China wangxinqd@sina.cn.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20150429
PL  - China
TA  - Acta Biochim Biophys Sin (Shanghai)
JT  - Acta biochimica et biophysica Sinica
JID - 101206716
RN  - 0 (Interleukin-1beta)
RN  - 0 (NF-kappa B)
RN  - 0 (Poly(ADP-ribose) Polymerase Inhibitors)
RN  - EC 2.4.2.30 (Poly(ADP-ribose) Polymerases)
SB  - IM
MH  - Cells, Cultured
MH  - Chondrocytes/*pathology
MH  - Humans
MH  - Inflammation/*prevention & control
MH  - Interleukin-1beta/*physiology
MH  - NF-kappa B/metabolism
MH  - Osteoarthritis/pathology/*physiopathology
MH  - Poly(ADP-ribose) Polymerase Inhibitors/*pharmacology
MH  - Poly(ADP-ribose) Polymerases/*drug effects
MH  - Real-Time Polymerase Chain Reaction
MH  - Reverse Transcriptase Polymerase Chain Reaction
OTO - NOTNLM
OT  - cartilage destruction
OT  - chondrocyte
OT  - inflammation response
OT  - interleukin-1beta
OT  - osteoarthritis
OT  - poly(ADP-ribose) polymerase 1
EDAT- 2015/05/01 06:00
MHDA- 2016/03/10 06:00
CRDT- 2015/05/01 06:00
PHST- 2014/12/12 00:00 [received]
PHST- 2015/03/03 00:00 [accepted]
PHST- 2015/05/01 06:00 [entrez]
PHST- 2015/05/01 06:00 [pubmed]
PHST- 2016/03/10 06:00 [medline]
AID - gmv033 [pii]
AID - 10.1093/abbs/gmv033 [doi]
PST - ppublish
SO  - Acta Biochim Biophys Sin (Shanghai). 2015 Jun;47(6):422-30. doi: 
      10.1093/abbs/gmv033. Epub 2015 Apr 29.