A1 Vertaisarvioitu alkuperäisartikkeli tieteellisessä lehdessä
Endothelial Cell Death and Intimal Foam Cell Accumulation in the Coronary Artery of Infected Hypercholesterolemic Minipigs
Tekijät: Birck MM, Saraste A, Hyttel P, Odermarsky M, Liuba P, Saukko P, Hansen AK, Pesonen E
Kustantaja: SPRINGER
Julkaisuvuosi: 2013
Journal: Journal of Cardiovascular Translational Research
Tietokannassa oleva lehden nimi: JOURNAL OF CARDIOVASCULAR TRANSLATIONAL RESEARCH
Lehden akronyymi: J CARDIOVASC TRANSL
Numero sarjassa: 4
Vuosikerta: 6
Numero: 4
Aloitussivu: 579
Lopetussivu: 587
Sivujen määrä: 9
ISSN: 1937-5387
DOI: https://doi.org/10.1007/s12265-013-9463-2
Tiivistelmä
Apoptosis of endothelial cells (ECs) has been suggested to play a role in atherosclerosis. We studied the synergism of hypercholesterolemia with Chlamydia pneumoniae and influenza virus infections on EC morphology and intimal changes in a minipig model. The coronary artery was excised at euthanasia (19 weeks of age) and serial sections were processed for the detection of EC apoptosis, histology, and transmission electron microscopy (TEM) studies. There was a significantly higher number of TUNEL-positive ECs in infected compared to noninfected groups [0.2942 % (interquartile ranges (IR), 0.2941; n = 26) versus 0 % (IR, 0; n = 12), p < 0.01]. Caspase-3 staining was negative. Cholesterol diet together with infections induced widening of the subendothelial space and appearance of increased numbers of foam cells. TEM revealed degenerative changes in cytoplasmic organelles and signs of EC necrosis. In conclusion, infection leads to an increase in coronary EC death and seems to exacerbate cholesterol-induced intimal thickening and foam cell accumulation.
Apoptosis of endothelial cells (ECs) has been suggested to play a role in atherosclerosis. We studied the synergism of hypercholesterolemia with Chlamydia pneumoniae and influenza virus infections on EC morphology and intimal changes in a minipig model. The coronary artery was excised at euthanasia (19 weeks of age) and serial sections were processed for the detection of EC apoptosis, histology, and transmission electron microscopy (TEM) studies. There was a significantly higher number of TUNEL-positive ECs in infected compared to noninfected groups [0.2942 % (interquartile ranges (IR), 0.2941; n = 26) versus 0 % (IR, 0; n = 12), p < 0.01]. Caspase-3 staining was negative. Cholesterol diet together with infections induced widening of the subendothelial space and appearance of increased numbers of foam cells. TEM revealed degenerative changes in cytoplasmic organelles and signs of EC necrosis. In conclusion, infection leads to an increase in coronary EC death and seems to exacerbate cholesterol-induced intimal thickening and foam cell accumulation.
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