PMID- 7639325
OWN - NLM
STAT- MEDLINE
DCOM- 19950912
LR  - 20181113
IS  - 0002-9440 (Print)
IS  - 1525-2191 (Electronic)
IS  - 0002-9440 (Linking)
VI  - 147
IP  - 2
DP  - 1995 Aug
TI  - Evidence for apoptosis in advanced human atheroma. Colocalization with 
      interleukin-1 beta-converting enzyme.
PG  - 251-66
AB  - This study sought evidence for apoptosis, a form of programmed cell death, in 
      human atheromatous coronary and carotid arteries. Markers for apoptotic cells 
      included in situ terminal deoxynucleotidyl transferase-mediated dUTP nick end 
      labeling (TUNEL), genomic DNA electrophoresis, and morphological analysis. 
      Intimal lesions contained more TUNEL+ cells (34 +/- 6%, n = 8) than 
      non-atherosclerotic arterial intima (8 +/- 3%, n = 5, P < 0.05). The tunica media 
      of the diseased arteries had a percentage of TUNEL+ cells (5 +/- 1%) similar to 
      that in the normal vessels (3 +/- 1%, N.S.). Oligonucleosomal DNA fragments were 
      visualized in extracts from 12 atheromatous plaques but in none of 5 
      non-atherosclerotic vessels. Both smooth muscle cells (SMC) and macrophages, two 
      major cell types in the atherosclerotic intima, bore markers of apoptosis, but 
      with different patterns, as determined by double histochemical labeling for cell 
      types and TUNEL. The TUNEL+ SMC localized mainly in the fibrotic portion of the 
      atheroma, whereas TUNEL+ macrophages clustered near or within the lipid-rich core 
      of the lesion. Atheromatous lesions expressed mRNA encoding interleukin-1 
      beta-converting enzyme (ICE), a mammalian cell death gene, as demonstrated by 
      reverse transcriptase polymerase chain reaction. Immunohistochemistry revealed 
      that ICE localized in regions of TUNEL+ SMC and macrophages. TUNEL- cells showed 
      little or no immunoreactive ICE. These data point to a role for apoptosis in 
      regulation of cell accumulation during atherogenesis and suggest involvement of 
      ICE in SMC death in fibrous regions of complex atheroma, and in macrophage death 
      in the lipid-rich core of the lesion. Apoptosis of vascular cells in fibrous cap 
      may impede maintenance or repair of the matrix in this region and affect 
      stability of the plaques.
FAU - Geng, Y J
AU  - Geng YJ
AD  - Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, 
      Boston, Massachusetts 02115, USA.
FAU - Libby, P
AU  - Libby P
LA  - eng
GR  - HL-34636/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Am J Pathol
JT  - The American journal of pathology
JID - 0370502
RN  - 0 (Biomarkers)
RN  - 0 (Oligonucleotide Probes)
RN  - 0 (RNA, Messenger)
RN  - EC 3.4.22.- (Cysteine Endopeptidases)
RN  - EC 3.4.22.36 (Caspase 1)
SB  - IM
CIN - Am J Pathol. 1995 Aug;147(2):229-34. PMID: 7639321
MH  - *Apoptosis
MH  - Arteries
MH  - Arteriosclerosis/genetics/*metabolism/*pathology
MH  - Base Sequence
MH  - Biomarkers
MH  - Caspase 1
MH  - Coronary Vessels/metabolism/pathology
MH  - Cysteine Endopeptidases/genetics/*metabolism
MH  - DNA Damage
MH  - Humans
MH  - Macrophages/pathology
MH  - Molecular Sequence Data
MH  - Muscle, Smooth, Vascular/pathology
MH  - Oligonucleotide Probes/genetics
MH  - RNA, Messenger/metabolism
MH  - Reference Values
MH  - Tissue Distribution
MH  - Tunica Intima/metabolism/pathology
PMC - PMC1869820
EDAT- 1995/08/01 00:00
MHDA- 1995/08/01 00:01
PMCR- 1996/02/01
CRDT- 1995/08/01 00:00
PHST- 1995/08/01 00:00 [pubmed]
PHST- 1995/08/01 00:01 [medline]
PHST- 1995/08/01 00:00 [entrez]
PHST- 1996/02/01 00:00 [pmc-release]
PST - ppublish
SO  - Am J Pathol. 1995 Aug;147(2):251-66.