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Thrombotic thrombocytopenic purpura and sporadic hemolytic-uremic syndrome
plasmas induce apoptosis in restricted lineages of human microvascular
endothelial cells
D Mitra, EA Jaffe, B Weksler, KA Hajjar, C Soderland and J Laurence
Department of Medicine, Cornell University Medical College, New York, NY
10021, USA.
Thrombotic thrombocytopenic purpura (TTP) and sporadic hemolytic-uremic
syndrome (HUS) are thrombotic microangiopathies that occur in the absence
of an inflammatory response. Ultrastructural features of tissues involved
in TTP/sporadic HUS suggest an apoptotic process. Consistent with these
findings, we observed that TTP plasmas induce apoptosis in primary human
endothelial cells (EC) of dermal microvascular but not umbilical vein
origin (Laurence et al, Blood 87:3245, 1996). We now document the ability
of plasmas from both TTP and sporadic HUS patients, but not from a patient
with childhood/diarrhea-associated HUS, to induce apoptosis and expression
of the apoptosis-associated molecule Fas (CD95) in restricted lineages of
microvascular EC. EC of small vessel dermal, renal, and cerebral origin
were susceptible to induction of Fas and an apoptotic cell death. In
contrast, microvascular EC of pulmonary and hepatic origin, as well as EC
of a large vessel, coronary artery, were resistant to both processes. This
dichotomy parallels the in vivo pathology of TTP/sporadic HUS, with notable
sparing of the pulmonary and hepatic microvasculature. Apoptotic EC also
had some features of a procoagulant phenotype, including depressed
production of prostaglandin I2 (prostacyclin). These phenomena support the
pathophysiologic significance of microvascular EC apoptosis in TTP, extend
it to a related disorder (sporadic HUS), and suggest consideration of
apoptosis inhibitors in the experimental therapeutics of these syndromes.
Volume 89,
Issue 4,
pp. 1224-1234,
02/15/1997
Copyright © 1997 by The American Society of Hematology
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