TY - JOUR
T1 - Primary cultures of human endothelial cells are susceptible to low doses of Shiga toxins and undergo apoptosis
AU - Yoshida, Tomoaki
AU - Fukada, Masako
AU - Koide, Naoki
AU - Ikeda, Hiroshi
AU - Sugiyama, Tsuyoshi
AU - Kato, Yutaka
AU - Ishikawa, Naohisa
AU - Yokochi, Takashi
N1 - Funding Information:
Received 16 February 1999; revised 26 July 1999; electronically published 12 November 1999. Informed consent was obtained from all subjects prior to participation in this study. Financial support: Ministry of Education, Japan (grant 10670274). Reprints or correspondence: Dr. Tomoaki Yoshida, Dept of Microbiology and Immunology, Aichi Medical University, Yazako, Nagakute, 480-1195 Aichi, Japan ([email protected]).
PY - 1999
Y1 - 1999
N2 - Various endothelial cells, with the exception of those from human microvasculatures, have been known to resist Shiga toxins (Stxs) in vitro. However, freshly prepared primary cultures of human endothelial cells from the umbilical vein and artery and the saphenous vein were shown to be killed by a very low dose of Stxs. This cytotoxicity of Stxs involves apoptosis, which seems to be caused by a mechanism distinct from the well-known action of Stxs to inhibit protein synthesis, since the blockade of protein synthesis by cycloheximide could not induce apoptosis or enhance the effect of Stxs. Passaged human endothelial cells have been found to be highly resistant to Stxs, which is consistent with previous reports, and not to show any evidence of apoptosis even when they are killed by a high dose of Stxs.
AB - Various endothelial cells, with the exception of those from human microvasculatures, have been known to resist Shiga toxins (Stxs) in vitro. However, freshly prepared primary cultures of human endothelial cells from the umbilical vein and artery and the saphenous vein were shown to be killed by a very low dose of Stxs. This cytotoxicity of Stxs involves apoptosis, which seems to be caused by a mechanism distinct from the well-known action of Stxs to inhibit protein synthesis, since the blockade of protein synthesis by cycloheximide could not induce apoptosis or enhance the effect of Stxs. Passaged human endothelial cells have been found to be highly resistant to Stxs, which is consistent with previous reports, and not to show any evidence of apoptosis even when they are killed by a high dose of Stxs.
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U2 - 10.1086/315116
DO - 10.1086/315116
M3 - Article
C2 - 10558968
AN - SCOPUS:0032735978
SN - 0022-1899
VL - 180
SP - 2048
EP - 2052
JO - Journal of Infectious Diseases
JF - Journal of Infectious Diseases
IS - 6
ER -