#5885 HYPOXIA INDUCES COMPLEMENT ACTIVATION ON HUMAN KIDNEY EPITHELIAL CELLS
نویسندگان
چکیده
Abstract Background and Aims Ischemia-reperfusion injury is an inevitable event associated with kidney transplantation (Tx) has a major impact on short- long-term graft survival. Proximal tubular epithelial cells are both source of complement during Tx target activation. The normal capacity to protect itself from activation through cellular expression regulatory proteins. In this study we investigated whether hypoxia reoxygenation increase C3 deposition alter protein (CD46, CD59 CD55). Method vitro, HKC-8 renal proximal were subjected 24h (1% O2) then reoxygenated for 4h (O2 = 21%) in the presence 40% human serum. qRT-PCR was used estimate level VEGF-A (as positive control), C3, CD46, CD55 expression. Similar analysis performed untreated, normoxic cells. Immunofluorescence staining determine cell surface intensity quantified by ImageJ. Experiments repeated three times. Results revealed significant increases after (p 0.0113). following increased insignificantly. Increased serum observed 0.026). However, no change seen CD46. Reoxygenation led significantly greater hypoxic compared (Figure 1, 2). Conclusion Our preliminary data suggests that surface. CD59, as one regulators upregulated at mRNA followed reperfusion These demonstrate activate system upregulation defence. CD46 do not change. Further needed identify regulation primary tissues.
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ژورنال
عنوان ژورنال: Nephrology Dialysis Transplantation
سال: 2023
ISSN: ['1460-2385', '0931-0509']
DOI: https://doi.org/10.1093/ndt/gfad063c_5885