PMID- 23547889
OWN - NLM
STAT- MEDLINE
DCOM- 20131112
LR  - 20191210
IS  - 1502-7732 (Electronic)
IS  - 0300-9742 (Linking)
VI  - 42
IP  - 5
DP  - 2013
TI  - Protective effect of allograft inflammatory factor-1 on the apoptosis of 
      fibroblast-like synoviocytes in patients with rheumatic arthritis induced by 
      nitro oxide donor sodium nitroprusside.
PG  - 349-55
LID - 10.3109/03009742.2013.772233 [doi]
AB  - OBJECTIVES: Inadequate apoptosis of rheumatic arthritis (RA) fibroblast-like 
      synoviocytes (FLS) plays a crucial role in the immunopathogenesis of RA. 
      Allograft inflammatory factor-1 (AIF-1) is a novel member of the cytokine network 
      that has been found to be involved in the immunological process underlying RA. 
      This study was undertaken to investigate the potential effects of AIF-1 on nitric 
      oxide donor (NO) sodium nitroprusside (SNP)-induced RA-FLS apoptosis, and the 
      possible molecular mechanisms underlying these effects. METHOD: FLS obtained from 
      patients with active RA were cultured in vitro and treated with SNP in the 
      present or absence of AIF-1. RA-FLS viability was tested by the 
      3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide (MTT) assay. RA-FLS 
      apoptosis was analysed by flow cytometry and terminal dUTP nick-end labeling 
      (TUNEL). The levels of phospho-Akt (p-Akt) and phospho-BAD (p-BAD) protein were 
      detected by Western blot. RESULTS: A 24-h AIF-1 pretreatment at concentrations 
      ranging from 10 to 100 ng/mL increased the viability of RA-FLS and prevented 
      RA-FLS apoptosis in a dose-dependent manner in the presence of SNP. AIF-1 induced 
      phosphorylation of Akt and BAD in a time- and concentration-dependent manner. The 
      effect was reversed by treatment with the PI3K inhibitor LY2940042 (LY) and the 
      nuclear factor kappa B (NF-kappaB) inhibitor pyrrolidine dithiocarbamate (PDTC). 
      CONCLUSIONS: AIF-1 can protect RA-FLS from apoptosis induced by NO by 
      upregulating the expression of p-Akt and p-BAD.
FAU - Liu, Y
AU  - Liu Y
AD  - Department of Rheumatology, Union Hospital, Tongji Medical College, Huazhong 
      University of Science and Technology , Wuhan , China.
FAU - Mei, C
AU  - Mei C
FAU - Du, R
AU  - Du R
FAU - Shen, L
AU  - Shen L
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130402
PL  - England
TA  - Scand J Rheumatol
JT  - Scandinavian journal of rheumatology
JID - 0321213
RN  - 0 (AIF1 protein, human)
RN  - 0 (Calcium-Binding Proteins)
RN  - 0 (Chromones)
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (Microfilament Proteins)
RN  - 0 (Morpholines)
RN  - 0 (Nitric Oxide Donors)
RN  - 0 (Pyrrolidines)
RN  - 0 (Thiocarbamates)
RN  - 169D1260KM (Nitroprusside)
RN  - 25769-03-3 (pyrrolidine dithiocarbamic acid)
RN  - 31M2U1DVID (2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one)
SB  - IM
MH  - Apoptosis/*drug effects
MH  - Calcium-Binding Proteins
MH  - Cell Survival/drug effects
MH  - Cells, Cultured
MH  - Chromones/pharmacology
MH  - DNA-Binding Proteins/*pharmacology
MH  - Drug Therapy, Combination
MH  - Enzyme Inhibitors/pharmacology
MH  - Female
MH  - Fibroblasts/drug effects/pathology
MH  - Health Status
MH  - Humans
MH  - Male
MH  - Microfilament Proteins
MH  - Middle Aged
MH  - Morpholines/pharmacology
MH  - Nitric Oxide Donors/*pharmacology
MH  - Nitroprusside/*pharmacology
MH  - Phosphorylation
MH  - Pyrrolidines/pharmacology
MH  - Rheumatic Fever/*pathology/physiopathology
MH  - Severity of Illness Index
MH  - Synovial Membrane/drug effects/*pathology
MH  - Thiocarbamates/pharmacology
EDAT- 2013/04/04 06:00
MHDA- 2013/11/13 06:00
CRDT- 2013/04/04 06:00
PHST- 2013/04/04 06:00 [entrez]
PHST- 2013/04/04 06:00 [pubmed]
PHST- 2013/11/13 06:00 [medline]
AID - 10.3109/03009742.2013.772233 [doi]
PST - ppublish
SO  - Scand J Rheumatol. 2013;42(5):349-55. doi: 10.3109/03009742.2013.772233. Epub 
      2013 Apr 2.