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肿瘤坏死因子α对大鼠肺微血管内皮细胞表达白细胞介素17受体C的影响 被引量：4

Effect of tumor necrosis factor-a on expression of interleukin-17 receptor C in pulmonary microvascular endothelial cells in rats
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摘要 目的观察肿瘤坏死因子a（TNF—a）对大鼠肺微血管内皮细胞表达白细胞介素17受体C（IL-17RC）的影响及甲泼尼龙的干预作用。方法体外培养肺微血管内皮细胞，根据TNF-a刺激浓度和时间的差异，将肺微血管内皮细胞分为TNF-a量效组和时效组：前者以0、0．1、1、10μg/LTNF—a与肺微血管内皮细胞孵育3h；后者以10μg／LTNF—a分别与肺微血管内皮细胞孵育0、1、3、6、12h。药物干预：分别以10μg／L的TNF．仅和200μg/L甲泼尼龙＋10μg／L的TNF-a与肺微血管内皮细胞孵育3h。用反转录-PCR，Western印迹及免疫细胞化学染色法检测IL-17RC表达。反转录-PCR检测TNF-a和甲泼尼龙对肺微血管内皮细胞表达IL-17RCmRNA的影响。结果反转录．PCR和Western印迹均证实肺微血管内皮细胞表达IL-17RC，免疫细胞化学染色发现IL-17RC主要分布在肺微血管内皮细胞胞膜和胞质。量效组IL-17RCmRNA相对表达量随TNF—a浓度（0、0．1、1、10μg／L）增加逐渐升高，分别为：0．241±0．010和0．372±0．017、0．452±0．017、0．643±0．042（F=46．460，P〈O．05）。时效组IL-17RCmRNA相对表达量于lh开始上升（0．417±0．038），3h达峰值（0．674±0．018），之后渐下降（6h：0．378±0．035，12h：0．318±0．032），但均高于孵育0h组（0．197±0．008），各时相组间比较差异均有统计学意义（F=37．903，P〈0．05）。甲泼尼龙显著下调TNF．仪诱导IL-17RCmRNA过度表达（0．333±0．031比0．660±0．026，F=89．637，P〈0．05）。结论IL-17RC主要分布在肺微血管内皮细胞胞膜和胞质；TNF-a刺激诱导肺微血管内皮细胞过度表达IL．17RC；甲泼尼龙抑制TNF—a对肺微血管内皮细胞表达IL-17RC的诱导效应，从而减轻肺微血管内皮细胞的炎症反应。 Objective To explore the effects of tumor necrosis factor-alpha （TNF-a） or methylprednisolone on the expression of interleukin-17 receptor C （IL-17RC） in rat pulmonary microvascular endothelial ceils （RPMVEC）. Methods Culture RPMVEC were randomly divided into dose-dependent and time-dependent groups. In dose-dependent group, cells were cultured with TNF-a （0, 0. 1, 1, 10 μg/L TNF-a） for 3 h. In time-dependent group, cells were cultured with TNF-a （ 10 μg/L） for 0, 1, 3, 6, 12 h. In the drug intervention group, cells were cultured with TNF-a （ 10 μg/L） or methylprednisolone （200 μg/L） ＋TNF-z （10 μg/L） for 3 h respectively. The expression of IL-17RC in isolated and cultured RPMVEC was identified by reverse transcription-polymerase chain reaction （RT-FCR）, Western blot and immunocytochemistry. The changes of IL-17RC mRNA were detected by RT-PCR after the stimulation of RPMVEC by TNF-a or rnethylprednisolone. Results RT-PCR and Western blot revealed that IL-17RC mRNA and protein were present in RPMVEC. The product of IL-17RC immunocytochemical reaction was predominantly located in cytoplasm and cytomembrane. In RPMVEC TNF-a significantly up-regulated IL- 17RC mRNA in a dose-dependent manner （0 μg/L TNF-agroup： 0. 241±0. 010, 0. 1 μg/L TNF-a group：0. 372 s 0. 017, 1 μg/L TNF-a group. 0. 452 s 0. 017, 10 μg,/L TNF-a group ： 0. 643 s 0. 042, F = 33.774, P 〈 0. 05）. In time-dependent group, the expression of IL-17RC mRNA rose at 1 h （0. 417 ± 0. 038）, peaked at 3 h （0. 674 s0. 018）, then decreased gradually at 6 h （0. 378 s0. 035） , but stayed higher at 12 h （0. 318 s0. 032）. When compared with 0 h group （0. 197 ±0. 008）, there were significant differences （F = 37. 903, P 〈 0. 05 ）. Methylprednisolone caused a marked attenuation of TNF-a-induced IL-17RC expression （0. 333 s 0. 031 vs 0. 660 s 0. 026, F = 89. 637, P 〈 0. 05 ）. Conclusions IL-17RC is predominantly present in cytomembrane and cytoplasm of RPMVEC. TNF-a up-regulates the expression of IL-17RC mRNA. Methylprednisolone inhibits the elevated expression of IL-17RC mRNA induced by TNF-a so as to relieve the inflammatory response of PMVEC.
作者 尤青海 张丹 孙耕耘 岳扬 王楠
机构地区 安徽医科大学第一附属医院呼吸内科
出处 《中华医学杂志》 CAS CSCD 北大核心 2013年第2期138-141,共4页 National Medical Journal of China
基金 国家自然科学基金（81070054,81100053）
关键词 肿瘤坏死因子仪 受体 白细胞介素17 内皮细胞 大鼠 Tumor necrosis factor-alpha Receptor, interleukin-17 Endothelial cells Rat
分类号 R346 [医药卫生—基础医学]
  • 相关文献

参考文献11

  • 1Kuestner RE, Taft DW, Haran A, et al. Identification of the IL- 17 receptor related molecule IL-17RC as the receptor for IL-17F. J Immunol, 2007, 179 : 5462-5473.
  • 2You QI-I, Sun GY, Wang N, et al. Interleukin-17F-induced pulmonary microvascular endothelial monolayer hyperpermeability via the protein kinase C pathway. J Surg Res, 2010, 162: 110- 121.
  • 3Mong PY, Petmlio C, Kaufman HL, et al. Activation of Rho kinase by TNF-ais required for JNK activation in human pulmonary micmvascular endothelial cells. J Immunol, 2008, 180: 550-558.
  • 4Shah NG, Tulapurkar ME, Damarla M, et al. Febrile-range hyperthermia augments reversible TNF-ot-induced hyperpermeahility in human microvascular lung endothelial cells. Int J Hyperthermia,2012, 28 : 627-635.
  • 5吴胜斌,王应灯,张薇.尿毒症患者血清对大鼠肺微血管内皮细胞单层通透性和骨架蛋白的影响[J].中华医学杂志,2008,88(47):3374-3377. 被引量：1
  • 6Ho AW, Shen F, Conti HR, et al. IL-17RC is required for immune signaling via an extended SEF/IL-R signaling domain in the cytoplasmic tail. J Immunol, 2010, 185: 1063-1070.
  • 7Roussel L, Houle F, Chan C, et al. IL-17 promotes p38 MAPK- dependent endothelial aetivation enhancing neutrophil recruitment to sites of inflammation. J Immunol, 2010, 184: 4531-4537.
  • 8Fujie H, Niu K, Ohba M, et al. A distinct regulatory role of Thl7 cytokines IL-17A and IL-17F in chemokine secretion from lung microvascular endothelial cells. Inflammation, 2012, 35 : 1119- 1131.
  • 9Sun SX, Ge BX, Miao CH. Effects of preconditioning with sevoflurane on TNF-ct-induced permeability and activation of p38 MAPK in rat pulmonary microvascular endothelial cells. Cell Biochem Biophys, 2011,61: 123-129.
  • 10Tang HF, Lu JJ, Tang JF, et al. Action of a Novel PDFA inhibitor ZL-n-91 on lipopolysaccharide-induced acute lung injury. Int Immunopharmacol, 2010, 10: 406-411.

二级参考文献15

  • 1王应灯,孙耕耘.灯盏花素对血小板活化因子致肺微血管内皮细胞损伤的影响[J].中国药理学通报,2004,20(7):780-783. 被引量：17
  • 2孙耕耘,王应灯.G蛋白偶联受体激酶2参与血小板活化因子致肺微血管内皮细胞损伤的机制[J].中华急诊医学杂志,2004,13(9):602-605. 被引量：10
  • 3高新庐,黎英,刘慧娟.26例尿毒症肺临床分析[J].中国血液净化,2005,4(6):332-332. 被引量：4
  • 4Hu G, Wang ZH, Zhuo HQ. Clinical analysis of 24 cases of uremic lung complications. Chin Crit Med ,2006,18 : 138.
  • 5Cheng C, Liu H, Ge H, et al. Lipopolysaccharide induces expression of SSeCKS in rat lung microvascular endothelial cell. Mol Cell Biochem,2007,305:1-8.
  • 6Parker JC, Stevens T, Randall J, et al. Hydraulic conductance of pulmonary microvascular and macrovascular endothelial cell monolayers. Am J Physiol Lung Cell Mol Physiol, 2006,291 : 30- 37.
  • 7Magee JC, Stone AE, Oldham KT, et al. Isolation, culture and characterization of rat lung microvascular endothelial cells. Am J Physiol, 1994,267:433-441.
  • 8Carpenter CL. Actin cytoskeleton and cell signaling. Crit Care Med,2000, 28:94-99.
  • 9Rabb H, Wang Z, Nemoto T, et al. Acute renal failure leads to dysregulation of lung salt and water channels. Kidney Int, 2003, 63:600-606.
  • 10Scheel PJ, Liu M, Rabb H. Uremic Lung: new insights into a forgotten condition. Kidney Int ,2008,74:849-851.

同被引文献32

  • 1Kuestner RE, Taft OW, Haran A, et al. Identification of the TL-17 receptor related molecule IL-l7RC as the receptor for IL-17F. J Immunol, 2007,179: 5462 -5473.
  • 2Haudenschild DR, Curtiss SB, Moseley TA, et al. Genera?tion of interleukin-l7 receptor-like protein (IL-17RL) in prostate by alternative splicing of RNA. Prostate, 2006, 66 : 1268 - 1274.
  • 3Ho AW, Gaffen SL. IL-l7RC: a partner in IL-17 signaling and beyond. Semin lmmunopathol. 2010,32 : 33 - 42.
  • 4Fujie H, Niu K, Ohba M, et al. A distinct regulatory role of Thl7 cytokines IL-l7 A and IL-l7 F in chemokine secretion from lung microvascular endothelial cells. Inflammation. 2012,35 : [lt9 - 1t3!.
  • 5Valente AJ, Yoshida T, Gardner JO. et al. Interleukin-17 A stimulates cardiac fibroblast proliferation and migration via negative regulation of the dual-specificity phosphatase MKP- 1I0USP-l. Cell Signal, 2012,24 : 560 -568.
  • 6Hirai Y,Iyoda M,Shibata T,et al. IL-17A stimulates granu?locyte colony-stimulating factor production via ERKlI2 but not p38 or JNK in human renal proximal tubular epithelial cells. Am J Physiol Renal Physiol,2012,302 : F244 - F250.
  • 7Liu L,Ge O,Ma L,et al. Interleukin-17 and prostaglandin E2 are involved in formation of an M2 macrophage-dominant mi?croenvironment in lung cancer. J Thorac Oncol, 2012, 7 : [091 - llOO.
  • 8Liu Y, Zhu H, Su Z, et al. IL-17 contributes to cardiac fi?brosis following experimental autoimmune myocarditis by a PKCfYErkll2/NF -KB-dependent signaling pathway. lnt Im?munol, 2012,24 : 605 -612.
  • 9Kudo M, Melton AC, Chen C, et al. IL-17 A produced by ex/3 T cells drives airway hyper-responsiveness in mice and enhances mouse and human airway smooth muscle contrac?tion. Nat Med, 2012,18: 547 -554.
  • 10Kang Z, Liu L, Spangler R, et al. IL-17 -induced actl-me?diated signaling is critical for cuprizone-induced demyelina?tion. J Neurosci, 2012,32 : 8284 -8292.

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二级引证文献8

中华医学杂志
2013年 第2期

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