PMID- 17241167
OWN - NLM
STAT- MEDLINE
DCOM- 20070403
LR  - 20220310
IS  - 0902-0055 (Print)
IS  - 0902-0055 (Linking)
VI  - 22
IP  - 1
DP  - 2007 Feb
TI  - Nitric oxide promotes the progression of periapical lesion via inducing 
      macrophage and osteoblast apoptosis.
PG  - 24-9
AB  - This study aimed to elucidate the modulation by nitric oxide (NO) of the 
      apoptosis of macrophages and osteoblasts, the essential cellular components in 
      the development of periapical lesions. Lipopolysaccharide (LPS) induced prominent 
      nitrite synthesis in J774 mouse macrophage cell lines. Exposure to LPS induced 
      obvious apoptosis in J774 cells, whereas transient transfection with murine 
      inducible nitric oxide synthase (iNOS), small interfering RNA (siRNA) diminished 
      this effect. Tumor necrosis factor-alpha (TNF-alpha) and 
      S-nitroso-N-acetyl-DL-penicillamine (SNAP) (a NO donor) triggered apoptosis in 
      UMR-106 rat osteoblastic cell lines and a synergistic effect was noted when 
      TNF-alpha and SNAP were added to the medium together. Administration of siRNAs 
      for c-Fos and c-Jun: components of activator protein-1 (AP-1) and transforming 
      growth factor-beta1 attenuated the combined effect markedly. Terminal 
      deoxynucleotidyl transferase-mediated nick end-labeling (TUNEL) stain in a rat 
      model of induced periapical lesion showed positive apoptotic signals in 
      macrophages and osteoblasts. Administration of N(G)-monomethyl-l-arginine 
      markedly diminished the extent of bone loss and the amounts of apoptotic 
      macrophages and osteoblasts. In conclusion, NO mediates LPS-stimulated apoptosis 
      of macrophages. It also induces osteoblast apoptosis and augments the 
      pro-apoptotic effect of cytokines. Inhibition of NO synthesis in vivo attenuates 
      apoptosis and the size of periapical lesions. Taken together, these results 
      suggest that NO may promote the progression of periapical lesion by inducing the 
      apoptosis of macrophages and osteoblasts.
FAU - Lin, S-K
AU  - Lin SK
AD  - Department of Dentistry, National Taiwan University Hospital, Taipei, Taiwan.
FAU - Kok, S-H
AU  - Kok SH
FAU - Lin, L-D
AU  - Lin LD
FAU - Wang, C-C
AU  - Wang CC
FAU - Kuo, M Y P
AU  - Kuo MY
FAU - Lin, C-T
AU  - Lin CT
FAU - Hsiao, M
AU  - Hsiao M
FAU - Hong, C-Y
AU  - Hong CY
LA  - eng
PT  - Journal Article
PL  - Denmark
TA  - Oral Microbiol Immunol
JT  - Oral microbiology and immunology
JID - 8707451
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (Free Radical Scavengers)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Nitric Oxide Donors)
RN  - 0 (Nitrites)
RN  - 0 (Proto-Oncogene Proteins c-fos)
RN  - 0 (Proto-Oncogene Proteins c-jun)
RN  - 0 (RNA, Small Interfering)
RN  - 27JT06E6GR (omega-N-Methylarginine)
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - 79032-48-7 (S-Nitroso-N-Acetylpenicillamine)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase Type II)
RN  - EC 1.14.13.39 (Nos2 protein, mouse)
MH  - Animals
MH  - Apoptosis/*drug effects
MH  - Cell Line
MH  - Cells, Cultured
MH  - Disease Models, Animal
MH  - Disease Progression
MH  - Drug Synergism
MH  - Enzyme Inhibitors/pharmacology
MH  - Free Radical Scavengers/*pharmacology
MH  - Lipopolysaccharides/pharmacology
MH  - Macrophages/*drug effects
MH  - Mice
MH  - Nitric Oxide/*pharmacology
MH  - Nitric Oxide Donors/pharmacology
MH  - Nitric Oxide Synthase Type II/pharmacology
MH  - Nitrites/metabolism
MH  - Osteoblasts/*drug effects
MH  - Periapical Diseases/*physiopathology
MH  - Proto-Oncogene Proteins c-fos/pharmacology
MH  - Proto-Oncogene Proteins c-jun/pharmacology
MH  - RNA, Small Interfering/pharmacology
MH  - Rats
MH  - Rats, Wistar
MH  - S-Nitroso-N-Acetylpenicillamine/pharmacology
MH  - omega-N-Methylarginine/pharmacology
EDAT- 2007/01/24 09:00
MHDA- 2007/04/04 09:00
CRDT- 2007/01/24 09:00
PHST- 2007/01/24 09:00 [pubmed]
PHST- 2007/04/04 09:00 [medline]
PHST- 2007/01/24 09:00 [entrez]
AID - OMI316 [pii]
AID - 10.1111/j.1399-302X.2007.00316.x [doi]
PST - ppublish
SO  - Oral Microbiol Immunol. 2007 Feb;22(1):24-9. doi: 
      10.1111/j.1399-302X.2007.00316.x.