Journal
BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
Volume 25, Issue 8, Pages 1486-1491Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.bbmt.2019.03.002
Keywords
Transplant-associated thrombotic microangiopathy; Complement; Heme oxygenase-1; Decay-accelerating factor; N-acetylcysteine
Categories
Funding
- National Nature Science Foundation of China [81620108001, 91439112, 91739302, 81270591, 81670132]
- Jiangsu Province of China [BK20131167, RC2011105]
- Jiangsu Provincial Special Program of Social Development [SBE2016740635]
- Jiangsu Provincial Special Program of Medical Science [BL2012005]
- Priority Academic Program Development of Jiangsu Higher Education Institutions
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Transplant-associated thrombotic microangiopathy (TA-TMA) is a severe complication in patients after hematopoietic stem cell transplantation. The pathogenesis of TA-TMA is still unclear. Previous studies showed that complement activation plays an important role in the development of TA-TMA. However, no data showed which kind of complement component triggers this process. In this study we found that heme oxygenase-1, which could induce decay-accelerating factor (DAF) and inhibit the membrane-attack complex, was significantly decreased in patients with TA-TMA. DAF levels in the TA-TMA group were in line with the levels in the myocardial infarction group but were lower than levels in the healthy, noncomplication, infection, and graft-versus-host disease groups (P < .05). Human umbilical vein endothelial cells (HUVECs) incubated with TA-TMA plasma showed lower DAF levels compared with that incubated with normal human plasma. Notably, treatment with N-acetylcysteine (NAC), a drug against oxidation, increased the level of DAF. NAC could also inhibit complement activation in HUVECs incubated with TA-TMA plasma. Taken together, we propose that NAC represents a new potential therapy for patients facing TA-TMA. (C) 2019 American Society for Blood and Marrow Transplantation.
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