摘要
目的 通过建立小鼠心脏及主动脉移植模型探讨Fas途径介导细胞凋亡在慢性排斥反应所致移植物血管病变形成中的作用。方法 (1)正常B6及B6.MRL(Fas -/-)→B10 .2R小鼠腹腔异位心脏移植。B10 .2R→B6小鼠胸主动脉异位移植。定期获取移植物。观察移植物存活率与组织形态学改变 ;TUNEL及FITC AnnexinV /PI双染色方法检测移植物中凋亡细胞形态及分布 ;B6小鼠主动脉体外培养。人重组的可溶性FasL诱导平滑肌细胞凋亡。结果 B6.MRL(Fas-/-)供体来源移植物存活期显著延长 ,其血管平滑肌细胞凋亡明显减少。新生血管内膜中的平滑肌细胞具有抗Fas介导凋亡的特性。
Obejective To study the role of Fas/FasL passway mediated apoptosis in transplant vasculopathy caused by chronic rejection in murine cardiac and aorta allograft.Methods Heart from B6 and B6.MRL (Fas-/-) mice was heterotopically grafted into B10.2R mice and aorta from B10.2R mice into B6 mice.The survival rate and histological changes were evaluated.Apoptosis was identified in histological sections by TUNEL assay and FITC Annexin V/PI double staining.Recombined soluble human FasL induced smooth muscle cell (SMC) apoptosis was demonstrated by in vitro co culture with B6 mice aorta segment.Results Fas deficiency could prolong cardiac graft survival.SMC apoptosis was reduced in the media of grafted B6.MRL hearts.Neointimal SMCs of aorta with chronic rejection were resistant to Fas mediated apoptosis.Conclusion Fas/FasL pathway induced apoptosis and the sensitivity of SMC to FasL induced apoptosis might play an important role in the development of transplant vasculopathy caused by chronic rejection.
出处
《中华实验外科杂志》
CAS
CSCD
北大核心
2003年第10期930-932,共3页
Chinese Journal of Experimental Surgery
基金
国家自然科学基金资助项目 (30 0 70 2 1 0 )
