Renal tubular epithelial cell apoptosis by Fas-FasL-dependent self-injury can augment renal allograft injury
Renal tubular epithelial cell apoptosis by Fas-FasL-dependent self-injury can augment renal allograft injury
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DOI：
10.1016/j.transproceed.2003.08.031
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发表时间：
2003-11-01
影响因子：
0.9
通讯作者：
Jevnikar, AM
中科院分区：
文献类型：
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作者：
Du, C;Guan, Q;Jevnikar, AM
由于肾小管上皮细胞（TEC）同时表达Fas和FasL，因此Fas-FasL相互作用在同种异体肾移植损伤中的作用可能是复杂的。TEC自伤的作用和调节尚未研究。在TEC，FasL承载，Fas无效TEC的共培养物中，被证明诱导TEC承载Fas的凋亡。与其2.6 +/-0.3%的基础水平相比，以10：1（E/T）的比率共培养效应子lpr-TEC（M3.1-lpr）与靶WT-TEC（CS3.7）诱导15.2 +/-2.4%的靶细胞凋亡。类似地，lpr-TEC在gld-TEC（MRM-gld）中诱导细胞凋亡，从3.7 +/- 0.2%的基础水平至6.4+/-0.3%。在肾移植模型中测试损伤时肾Fas-FasL的表达。与正常（野生型[WT]）C3 H/Hej供体相比，C57 BL/6（B6）小鼠移植了Fas缺陷型C3 H-lpr/lpr或FasL突变型C3 H gld/gld肾脏。与WT供者相比，lpr和gld受者的生存率均有所提高（P
The role of Fas-FasL interactions in kidney allograft injury may be complex as renal tubular epithelial cells (TEC) express both Fas and FasL. The role and regulation of TEC self-injury has not been investigated. In co-cultures of TEC, FasL-bearing, Fas-null TEC was demonstrated to induce apoptosis of TEC-bearing Fas. Co-culturing effector lpr-TEC (M3.1-lpr) with target WT-TEC (CS3.7) at a ratio of 10:1 (E/T) induced 15.2 +/- 2.4% of target apoptosis as compared to its basal level of 2.6 +/- 0.3%. Similarly lpr-TEC induced apoptosis in gld-TEC (MRM-gld) from a basal level of 3.7 +/- 0.2% to 6.4+/- 0.3%. Expression of kidney Fas-FasL on injury was tested in a renal transplant model. C57BL/6(B6) mice were transplanted with Fas-deficient C3H-lpr/lpr or FasL mutation C3H gld/gld kidneys as compared to normal (wild-type [WT]) C3H/Hej donors. Survival of both lpr and gld recipient was improved compared to WT donors (P