• 復(fù)旦大學(xué)附屬中山醫(yī)院上海市心血管病研究所 心血管外科,上海 200032;

目的 探討終末期腎?。‥SRD)患者冠狀動脈旁路移植術(shù)(CABG)前大隱靜脈橋血管中細(xì)胞外基質(zhì) (ECM)基因表達(dá)的特點(diǎn)?!》椒ā∵x擇復(fù)旦大學(xué)附屬中山醫(yī)院自2004年7月至2010年12月期間收治的經(jīng)冠狀動脈造影明確診斷為冠心病患者68例進(jìn)行研究,將68例患者按術(shù)前有無ESRD史,篩選出ESRD患者30例作為ESRD組(需維持性血液透析患者),38例無腎病史患者作為對照組。收集整理所有入選患者詳細(xì)的術(shù)前臨床資料;術(shù)中收集大隱靜脈標(biāo)本,以基因芯片、免疫組織化學(xué)和蛋白印跡法(Western blotting)闡明ESRD條件下CABG術(shù)前大隱靜脈橋血管中細(xì)胞外基質(zhì)基因表達(dá)的情況。 結(jié)果 兩組術(shù)前臨床資料除腎病相關(guān)數(shù)據(jù)外,其余臨床資料差異無統(tǒng)計(jì)學(xué)意義(P>0.05)。ESRD組患者CABG術(shù)前大隱靜脈橋血管中細(xì)胞外基質(zhì)相關(guān)基因表達(dá)上調(diào) 3倍以上的基因有16個(gè),而表達(dá)下調(diào)3倍以上的基因則有3個(gè);ESRD組基質(zhì)金屬蛋白酶-2 (MMP-2)、基質(zhì)金屬蛋白酶-9 (MMP-9) 活性較對照組升高(2.60± 0.50 vs. 0.70±0.16,1.80±0.40 vs. 0.60±0.15,P<0.01),而組織型基質(zhì)金屬蛋白酶抑制劑-2 (TIMP-2) 和組織型基質(zhì)金屬蛋白酶抑制劑-3 (TIMP-3) 活性較對照組降低(0.60±0.19 vs. 2.20±0.30,0.90±0.28vs. 2.40±0.70,P< 0.05)?!〗Y(jié)論 與ESRD相關(guān)的多種心血管病危險(xiǎn)因素,嚴(yán)重影響CABG術(shù)前大隱靜脈橋血管中細(xì)胞外基質(zhì)基因表達(dá)平衡,并且這種平衡的打破,有促進(jìn)CABG術(shù)后靜脈橋血管病變發(fā)生的危險(xiǎn)。

引用本文: 孫勇新,丁文軍,朱黎鳴,史昀青,魏強(qiáng),王春生. 終末期腎病患者大隱靜脈橋血管中 細(xì)胞外基質(zhì)相關(guān)基因表達(dá)的特點(diǎn). 中國胸心血管外科臨床雜志, 2013, 20(1): 81-86. doi: 復(fù)制

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2.  Yerram P, Karuparthi PR, Hesemann L, et al. Chronic kidney disease and cardiovascular risk. J Am Soc Hypertens, 2007, 1 (3):178-184.
3.  Goldman S, Zadina K, Moritz T, et al. Long-term patency of saphe nous vein and left internal mammary artery grafts after coronary  artery bypass surgery:results from a Department of Veterans Affairs Cooperative Study. J Am Coll Cardiol, 2004, 44 (11):2149-2156.
4.  George SJ, Wan S, Hu J, et al. Sustained reduction of vein graft neointima formation by ex vivo TIMP-3 gene therapy.  Circulation, 2011, 124 (11 Suppl):S135-S142.
5.  Dummler S, Eichhorn S, Tesche C, et al. Pulsatile ex vivo perfusion of human saphenous vein grafts under controlled pressure conditions increases MMP-2 expression. Biomed Eng Online, 2011, 10 (7):62-67.
6.  Szczech LA, Reddan DN, Owen WF, et al. Differential survival after coronary revascularization procedures among patients with renal insufficiency. Kidney Int, 2001, 60 (1):292-299.
7.  Orii K, Hioki M, Iedokoro Y, et al. Prognostic factors affecting clinical outcomes after coronary artery bypass surgery:analysis of patients with chronic kidney disease after 5.9 years of follow-up. J Nippon Med Sch, 2011, 78 (3):156-165.
8.  Koh KH, Tan C, Hii L, et al. Outcome of coronary artery bypass grafting in end stage renal disease patients. Med J Malaysia, 2012, 67 (2):173-176.
9.  Turner NA, Ho S, Warburton P, et al. Smooth muscle cells cultured from human saphenous vein exhibit increased proliferation, invasion, and mitogen-activated protein kinase activation in vitro compared with paired internal mammary artery cells. J Vasc Surg, 2007, 45 (5):1022-1028.
10.  Mitra AK, Jia G, Gangahar DM, et al. Temporal PTEN inactivation causes proliferation of saphenous vein smooth muscle cells of human CABG conduits. J Cell Mol Med, 2009, 13 (1):177-187.
11.  Mangi AA, Dzau VJ. Gene therapy for human bypass grafts. Ann Med, 2001, 33 (3):153-155.
12.  NI Jun, Waldman A, Khachigian LM. c-Jun regulates shear- and injury-inducible Egr-1 expression, vein graft stenosis after autologous end-to-side transplantation in rabbits, and intimal hyperplasia in human saphenous veins. J Biol Chem, 2010, 285 (6):4038-4048.
13.  Turner NA, Hall KT, Ball SG, et al. Selective gene silencing of either MMP-2 or MMP-9 inhibits invasion of human saphenous vein smooth muscle cells. Atherosclerosis, 2007, 193 (1):36-43.
14.  Corpataux JM, Naik J, Porter KE, et al. A comparison of six statins on the development of intimal hyperplasia in a human vein culture model. Eur J Vasc Endovasc Surg, 2005, 29 (2):177-181.
15.  Sunagawa G, Komiya T, Tamura N, et al. Coronary artery bypass surgery is superior to percutaneous coronary intervention with drug-eluting stents for patients with chronic renal failure on hemodialysis. Ann Thorac Surg, 2010, 89 (6):1896-1900.
16.  Panichi V, Scatena A, Migliori M, et al. Biomarkers of chronic inflammatory state in uremia and cardiovascular disease. Int J Inflam, 2012, 2012:360147.
  1. 1.  Foley RN, Parfrey PS, Sarnak MJ. Clinical epidemiology of cardiovascular disease in chronic renal disease. Am J Kidney Dis, 1998, 32 (5):S112-S119.
  2. 2.  Yerram P, Karuparthi PR, Hesemann L, et al. Chronic kidney disease and cardiovascular risk. J Am Soc Hypertens, 2007, 1 (3):178-184.
  3. 3.  Goldman S, Zadina K, Moritz T, et al. Long-term patency of saphe nous vein and left internal mammary artery grafts after coronary  artery bypass surgery:results from a Department of Veterans Affairs Cooperative Study. J Am Coll Cardiol, 2004, 44 (11):2149-2156.
  4. 4.  George SJ, Wan S, Hu J, et al. Sustained reduction of vein graft neointima formation by ex vivo TIMP-3 gene therapy.  Circulation, 2011, 124 (11 Suppl):S135-S142.
  5. 5.  Dummler S, Eichhorn S, Tesche C, et al. Pulsatile ex vivo perfusion of human saphenous vein grafts under controlled pressure conditions increases MMP-2 expression. Biomed Eng Online, 2011, 10 (7):62-67.
  6. 6.  Szczech LA, Reddan DN, Owen WF, et al. Differential survival after coronary revascularization procedures among patients with renal insufficiency. Kidney Int, 2001, 60 (1):292-299.
  7. 7.  Orii K, Hioki M, Iedokoro Y, et al. Prognostic factors affecting clinical outcomes after coronary artery bypass surgery:analysis of patients with chronic kidney disease after 5.9 years of follow-up. J Nippon Med Sch, 2011, 78 (3):156-165.
  8. 8.  Koh KH, Tan C, Hii L, et al. Outcome of coronary artery bypass grafting in end stage renal disease patients. Med J Malaysia, 2012, 67 (2):173-176.
  9. 9.  Turner NA, Ho S, Warburton P, et al. Smooth muscle cells cultured from human saphenous vein exhibit increased proliferation, invasion, and mitogen-activated protein kinase activation in vitro compared with paired internal mammary artery cells. J Vasc Surg, 2007, 45 (5):1022-1028.
  10. 10.  Mitra AK, Jia G, Gangahar DM, et al. Temporal PTEN inactivation causes proliferation of saphenous vein smooth muscle cells of human CABG conduits. J Cell Mol Med, 2009, 13 (1):177-187.
  11. 11.  Mangi AA, Dzau VJ. Gene therapy for human bypass grafts. Ann Med, 2001, 33 (3):153-155.
  12. 12.  NI Jun, Waldman A, Khachigian LM. c-Jun regulates shear- and injury-inducible Egr-1 expression, vein graft stenosis after autologous end-to-side transplantation in rabbits, and intimal hyperplasia in human saphenous veins. J Biol Chem, 2010, 285 (6):4038-4048.
  13. 13.  Turner NA, Hall KT, Ball SG, et al. Selective gene silencing of either MMP-2 or MMP-9 inhibits invasion of human saphenous vein smooth muscle cells. Atherosclerosis, 2007, 193 (1):36-43.
  14. 14.  Corpataux JM, Naik J, Porter KE, et al. A comparison of six statins on the development of intimal hyperplasia in a human vein culture model. Eur J Vasc Endovasc Surg, 2005, 29 (2):177-181.
  15. 15.  Sunagawa G, Komiya T, Tamura N, et al. Coronary artery bypass surgery is superior to percutaneous coronary intervention with drug-eluting stents for patients with chronic renal failure on hemodialysis. Ann Thorac Surg, 2010, 89 (6):1896-1900.
  16. 16.  Panichi V, Scatena A, Migliori M, et al. Biomarkers of chronic inflammatory state in uremia and cardiovascular disease. Int J Inflam, 2012, 2012:360147.