PMID- 11139364
OWN - NLM
STAT- MEDLINE
DCOM- 20010222
LR  - 20171116
IS  - 1089-8603 (Print)
IS  - 1089-8603 (Linking)
VI  - 4
IP  - 6
DP  - 2000 Dec
TI  - Expression of inducible nitric oxide synthase and Fas/Fas ligand correlates with 
      the incidence of apoptotic cell death in atheromatous plaques of human coronary 
      arteries.
PG  - 561-71
AB  - It was recently reported that inducible nitric oxide synthase was expressed in 
      advanced atheromatous plaques. So we investigated the effect of NO or 
      peroxynitrite reactive product of NO or O(2)(-) released by iNOS induced in 
      macrophages or T lymphocytes on inflammatory cells in atheromatous plaques of 
      human coronary arteries by immunohistochemistry. We found that iNOS was expressed 
      in T lymphocytes and macrophages in T lymphocytes and macrophages coexisted 
      advanced atheromatous areas. Most of the smooth muscle cells are not coexisted 
      with T lymphocytes. We could not find iNOS in those smooth muscle cells. Only a 
      small number of iNOS-positive smooth muscle cells were found close to T 
      lymphocytes and macrophages. Markers for apoptotic cells induced in situ terminal 
      deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) showed that 
      many apoptotic T lymphocytes and macrophages existed near iNOS induced cells. Fas 
      and Fas ligand were expressed in almost same areas that iNOS was expressed. By 
      double-label immunostaining, Fas was expressed in T lymphocytes but Fas ligand 
      was expressed in macrophages and in some T lymphocytes. These results suggest 
      that NO from iNOS induces Fas and Fas ligand-mediated apoptosis and associates 
      with regression of atherosclerosis. On the other hand, nitrotyrosine was detected 
      wider areas than iNOS. So peroxynitrite from iNOS damages cells and tissues 
      widely and may associate with progression of atherosclerosis. These results 
      suggest an important role of iNOS in mediating both regressive changes and 
      progressive change in atheromatous plaques.
CI  - Copyright 2000 Academic Press.
FAU - Esaki, T
AU  - Esaki T
AD  - Department of Geriatrics, Nagoya University School of Medicine, 65 Turuma-cho, 
      Showa-ku, Nagoya 466, Japan. tesaki@ucla.edu
FAU - Hayashi, T
AU  - Hayashi T
FAU - Muto, E
AU  - Muto E
FAU - Kano, H
AU  - Kano H
FAU - Kumar, T N
AU  - Kumar TN
FAU - Asai, Y
AU  - Asai Y
FAU - Sumi, D
AU  - Sumi D
FAU - Iguchi, A
AU  - Iguchi A
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Nitric Oxide
JT  - Nitric oxide : biology and chemistry
JID - 9709307
RN  - 0 (FASLG protein, human)
RN  - 0 (Fas Ligand Protein)
RN  - 0 (Membrane Glycoproteins)
RN  - 0 (fas Receptor)
RN  - 3604-79-3 (3-nitrotyrosine)
RN  - 42HK56048U (Tyrosine)
RN  - EC 1.14.13.39 (NOS2 protein, human)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase Type II)
SB  - IM
MH  - Aged
MH  - Aged, 80 and over
MH  - Apoptosis
MH  - Coronary Artery Disease/*metabolism/pathology
MH  - Coronary Vessels/*metabolism/pathology
MH  - Fas Ligand Protein
MH  - Female
MH  - Humans
MH  - Immunohistochemistry
MH  - In Situ Nick-End Labeling
MH  - Male
MH  - Membrane Glycoproteins/*metabolism
MH  - Nitric Oxide Synthase/*metabolism
MH  - Nitric Oxide Synthase Type II
MH  - Tyrosine/*analogs & derivatives/metabolism
MH  - fas Receptor/*metabolism
EDAT- 2001/01/05 11:00
MHDA- 2001/03/03 10:01
CRDT- 2001/01/05 11:00
PHST- 2001/01/05 11:00 [pubmed]
PHST- 2001/03/03 10:01 [medline]
PHST- 2001/01/05 11:00 [entrez]
AID - S1089-8603(00)90311-2 [pii]
AID - 10.1006/niox.2000.0311 [doi]
PST - ppublish
SO  - Nitric Oxide. 2000 Dec;4(6):561-71. doi: 10.1006/niox.2000.0311.