中华医学杂志
中華醫學雜誌
중화의학잡지
National Medical Journal of China
2012年
42期
2976-2979
,共4页
武多娇%钱梦佳%戎瑞明%许明%朱同玉
武多嬌%錢夢佳%戎瑞明%許明%硃同玉
무다교%전몽가%융서명%허명%주동옥
移植物排斥%蛋白质阵列分析%炎症%细胞因子%网络
移植物排斥%蛋白質陣列分析%炎癥%細胞因子%網絡
이식물배척%단백질진렬분석%염증%세포인자%망락
Graft rejection%Protein array analysis%Inflammation%Cytokine%Network
目的 探讨肾移植后急性排斥反应中炎症相关因子的表达变化及蛋白网络的功能.方法 收集肾移植后急性排斥反应患者及肾功能稳定患者血清样本,各6例；应用APIX蛋白芯片技术检测40个炎症相关细胞因子,寻找两组间表达水平差异具有统计学意义的细胞因子.并应用String和Network Ontology Analysis在线工具构建差异蛋白相互作用网络,分析其生物功能.结果 在急性排斥反应及肾功能稳定患者的血清中有8个细胞因子的表达水平差异有统计学意义[嗜酸细胞活化趋化因子2(CCL24):700(255 ～ 1157)比330(100 ～ 610) ng/L；细胞间黏附分子1(ICAM-1):58 737(8018～ 10 5395)比22 660(137 ～68 914) ng/L;白细胞介素10(IL-10):120(20 ～517)比298(81 ～ 11 609) ng/L；IL-6可溶性受体(IL-6sR):11 328(3357～21 251)比7665 (370 ～ 12 455) ng/L；单核细胞炎性蛋白1α(CCL3):1712(7002 ～ 32 634)比283(54～1915) ng/L；单核细胞炎性蛋白1β(CCL4):554 (28～ 2355)和283(104～ 1915) ng/L；基质金属蛋白酶组织抑制因子1(TIMP-1):15 560(13 343 ～42 481)比11 271(1207 ～18 228) ng/L；正常T细胞表达和分泌因子(CCL5):44 547(38 252 ～78 631)比27 765(12 073 ～46 627) ng/L,均P＜0.05].蛋白相互作用及网络分析显示这些蛋白彼此联系,参与趋化、化学趋化、炎症反应、创伤应答及白细胞迁移等病理生理过程.结论 寻找肾移植急性排斥反应患者差异表达的炎症相关细胞因子并分析蛋白相互作用网络,有助于阐明肾移植急性排斥反应发病机制；差异蛋白可作为肾移植急性排斥反应候选诊断标志物或干预靶标.
目的 探討腎移植後急性排斥反應中炎癥相關因子的錶達變化及蛋白網絡的功能.方法 收集腎移植後急性排斥反應患者及腎功能穩定患者血清樣本,各6例；應用APIX蛋白芯片技術檢測40箇炎癥相關細胞因子,尋找兩組間錶達水平差異具有統計學意義的細胞因子.併應用String和Network Ontology Analysis在線工具構建差異蛋白相互作用網絡,分析其生物功能.結果 在急性排斥反應及腎功能穩定患者的血清中有8箇細胞因子的錶達水平差異有統計學意義[嗜痠細胞活化趨化因子2(CCL24):700(255 ～ 1157)比330(100 ～ 610) ng/L；細胞間黏附分子1(ICAM-1):58 737(8018～ 10 5395)比22 660(137 ～68 914) ng/L;白細胞介素10(IL-10):120(20 ～517)比298(81 ～ 11 609) ng/L；IL-6可溶性受體(IL-6sR):11 328(3357～21 251)比7665 (370 ～ 12 455) ng/L；單覈細胞炎性蛋白1α(CCL3):1712(7002 ～ 32 634)比283(54～1915) ng/L；單覈細胞炎性蛋白1β(CCL4):554 (28～ 2355)和283(104～ 1915) ng/L；基質金屬蛋白酶組織抑製因子1(TIMP-1):15 560(13 343 ～42 481)比11 271(1207 ～18 228) ng/L；正常T細胞錶達和分泌因子(CCL5):44 547(38 252 ～78 631)比27 765(12 073 ～46 627) ng/L,均P＜0.05].蛋白相互作用及網絡分析顯示這些蛋白彼此聯繫,參與趨化、化學趨化、炎癥反應、創傷應答及白細胞遷移等病理生理過程.結論 尋找腎移植急性排斥反應患者差異錶達的炎癥相關細胞因子併分析蛋白相互作用網絡,有助于闡明腎移植急性排斥反應髮病機製；差異蛋白可作為腎移植急性排斥反應候選診斷標誌物或榦預靶標.
목적 탐토신이식후급성배척반응중염증상관인자적표체변화급단백망락적공능.방법 수집신이식후급성배척반응환자급신공능은정환자혈청양본,각6례；응용APIX단백심편기술검측40개염증상관세포인자,심조량조간표체수평차이구유통계학의의적세포인자.병응용String화Network Ontology Analysis재선공구구건차이단백상호작용망락,분석기생물공능.결과 재급성배척반응급신공능은정환자적혈청중유8개세포인자적표체수평차이유통계학의의[기산세포활화추화인자2(CCL24):700(255 ～ 1157)비330(100 ～ 610) ng/L；세포간점부분자1(ICAM-1):58 737(8018～ 10 5395)비22 660(137 ～68 914) ng/L;백세포개소10(IL-10):120(20 ～517)비298(81 ～ 11 609) ng/L；IL-6가용성수체(IL-6sR):11 328(3357～21 251)비7665 (370 ～ 12 455) ng/L；단핵세포염성단백1α(CCL3):1712(7002 ～ 32 634)비283(54～1915) ng/L；단핵세포염성단백1β(CCL4):554 (28～ 2355)화283(104～ 1915) ng/L；기질금속단백매조직억제인자1(TIMP-1):15 560(13 343 ～42 481)비11 271(1207 ～18 228) ng/L；정상T세포표체화분비인자(CCL5):44 547(38 252 ～78 631)비27 765(12 073 ～46 627) ng/L,균P＜0.05].단백상호작용급망락분석현시저사단백피차련계,삼여추화、화학추화、염증반응、창상응답급백세포천이등병리생리과정.결론 심조신이식급성배척반응환자차이표체적염증상관세포인자병분석단백상호작용망락,유조우천명신이식급성배척반응발병궤제；차이단백가작위신이식급성배척반응후선진단표지물혹간예파표.
Objective To explore the changes of inflammation cytokines during acute renal transplantation rejection and decipher the functions of their protein-protein interaction network.Methods Serum samples were collected from renal transplantation patients with stable renal function or acute rejection (n =6 each) to measure the expression level of 40 inflammatory factors by APIX protein array.The differentially expressed proteins were selected and their protein-protein interaction networks constructed.And biologic processes were analyzed by the online tools of String and Network Ontology Analysis.Results There were 8 differentially expressed cytokines in the AR group versus the stable group(M (Q1-Q3),CCL24∶700(255-1157)vs 330(100-610)ng/L,ICAM-1:58 737 (8018-105 395) vs 22 660 (137-68 914) ng/L,IL-10∶120(20-517) vs 298 (81-11 609) ng/L,IL-6sR:11 328(3357-21 251) vs 7665(370-12 455)ng/L,CCL3:1712(7002-32 634) vs 283(54-1915) ng/L,CCL4:554 (28-2355) vs 283(104-1915)ng/L,TIMP-1:15 560 (13 343-42 481) vs 11 271(1207-18 228) ng/L,CCL5:44 547(38 252-78 631) vs 27 765 (12 073-46 627) ng/L,all P ＜ 0.05).The analyses of protein-protein association network showed that these proteins were correlated and involved in such biological processes as taxis,chemotaxis,inflammatory reactions,wound responses and leukocytic migration.Conclusions Comparing the inter-group differences of inflammatory cytokines and further developing and analyzing the protein-protein interaction network may help us to explore the mechanisms of acute renal transplantation rejection.And the differential cytokines can be used as candidate diagnostic biomarkers and intervention targets.
