[Ultrastructural changes in isolated cardiomyocytes in modeling of endoplasmic reticulum stress].
At modeling of endoplasmatic reticulum (ER) stress by it classic inducer thapsigargin, anoxia-reoxygenation and simultaneous inhibition ofproteasomal proteolysis, autophagy and apoptosis a diversity of ultrastructural peculiarities was shown. Their comparison allows to make a conclusion that changes in these groups of experiments are similar and typical for ER stress. Thapsigargin application was shown to result in accumulation of giant mitochondria in perinuclear zone of cardiomyocytes. Some of these mitochondria had destroyed and high condensed matrix. The structure of ER was normal but in some regions of cells the dilation of ER cisterns occurred that, to our opinion, is an essential sign of ER stress. In another group of cells thapsigargin caused dehydratation and osmiophilia of cytoplasm, significant dilation of ER cisterns, partial or complete degranulation of these organelles that often formed vacuoles with high electron density material. Also, the significant decrease of the number and size of mitochondria that had partially destroyed and condensed matrix was observed in these cells. The accumulation of lipofuscin and myophilament destruction at preservation of sarcoplasmic membrane integrity was detected. However, in conditions of simultaneous inhibition ofproteasomal proteolysis, aytophagy and apoptosis the loss of membrane integrity was shown, and we propose that it unconditionally should cause necrotic cell death. That was confirmed by use of fluorogenic dyes to detect necrosis and apoptosis. Our data indicate the important role of ER stress in processes of cardiomyocytes death at anoxia-reoxygenation and inhibition of proteasomal and autophagic proteolysis.
Tumanovs'ka
L V
LV
Nahibin
V S
VS
Dosenko
V Ie
VIe
Moĭbenko
O O
OO