| 1 | Interplay of neuropilin-1 and semaphorin 3A after partial hepatectomy in rats显示文摘AIM:To elucidate the role of neuropilin-1(Nrp-1) and semaphorin 3A(Sema3A) in sinusoidal remodeling during liver regeneration in rats.METHODS:Male Wistar/ST rats at 7 wk of age,weighing about 200 g,were used for all animal experiments.In vivo,at 24,48,72,96,144 and 192 h after twothirds partial hepatectomy(PHx),the remnant livers were removed.Liver tissues were immunohistochemically stained for Nrp-1,Sema3A and SE-1,a liver sinusoidal endothelial cell(SEC) marker.Total RNA of the liver tissue was extracted and reversely transcribed into cDNA.The mRNA expression of Sema3A was analyzed by quantitative real-time polymerase chain reaction and normalized to that of ribosomal protein S18.In vitro,SECs were isolated from rat liver and cultured in endothelial growth medium containing 20 ng/mL vascular endothelial cell growth factor.Migration of SECs in primary culture was assessed by cell transwell assay with or without recombinant Sema3A.Apoptotic cells were determined by a terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labeling method.RESULTS:In vitro,immunohistochemistry study revealed that Sema3A and Nrp-1 were constitutively expressed in hepatocytes and SECs,respectively,in normal rat liver tissues.Nrp-1 expression in SECs was quantified by the percentage of immunostained area with antiNrp-1 antibody in relation to the area stained with SE-1.Between 24 h and 96 h following resection of liver,Nrp-1 expression in SECs was transiently increased.Compared with the baseline(5.2% ± 0.1%),Nrp-1 expression in SECs significantly increased at 24 h(17.3% ± 0.7%,P < 0.05),48 h(39.1% ± 0.6%,P < 0.01),72 h(46.9% ± 4.5%,P < 0.01) and 96 h(29.9% ± 3.8%,P < 0.01) after PHx,then returned to the basal level at termination of liver regeneration.Interestingly,the expression of Sema3A was inversely associated with that of Nrp-1 in liver after PHx.Sema3A mRNA expression was significantly reduced by about 75% over the period 24-144 h after PHx(P < 0.05),and returned to basal levels at 192 h after PHx.In vitro,SECs isolated from rats after PHx(PHx-SECs) were observed to migrate to the lower chamber of the cell transwell system after incubation for 24 h,but not cells from normal rats(CONT-SECs),indicating that mobility of PHx-SECs increases as compared with that of CONT-SECs.Moreover,recombinant Sema3A significantly attenuated migration in PHx-SECs in primary culture(vehicle-treated 100% ± 7.9% vs Sema3A-treated 42.6% ± 5.4%,P < 0.01),but not in CONT-SECs.Compared with CONTSECs,the apoptotic rate of PHx-SECs decreased by 78.3%(P < 0.05).There was no difference in apoptosis between CONT-SECs that were treated with vehicle and Sema3A.However,in PHx-SECs,apoptosis was induced by the presence of 5 nmol Sema3A for 24 h(vehicle-treated 21.7% ± 7.6% vs Sema3A-treated 104.3% ± 8.9%,P < 0.05).In addition,immunohistochemistry confirmed the increased expression of Nrp-1 in PHx-SECs,while it was noted to a lesser extent in CONT-SECs.CONCLUSION:The interplay of Nrp-1 and Sema3A shown in our results may lead to a better understanding of interaction between sinusoidal remodeling and SECs during liver regeneration. | Ling Fu Tsuneo Kitamura Kazuhisa Iwabuchi Syozo Ichinose Mitsuaki Yanagida Hideoki Ogawa Sumio Watanabe Toshihide Maruyama Masafumi Suyama Kenji Takamori | 2012 | World Journal of Gastroenterology2012，18，36： | 5 |
| 2 | 骨髓移植后肝静脉闭塞病模型的鉴定及机制探讨显示文摘目的建立异基因骨髓移植后肝静脉闭塞病(HVOD)模型并探索其发生机制。方法将Balb/c小鼠随机分为3组,即生理盐水对照组(NS组)、单纯照射组和单纯骨髓移植组。于移植后第0、5、10、15和20天检测各组小鼠肝重、外周血胆红素总量(TBi1)以及外周血肿瘤坏死因子a(TNF-a)、白细胞介素6(IL-6)和单核细胞趋化因子-1(MCP-1)浓度的变化,小鼠肝脏组织病理学改变。结果小鼠肝重和TBi1均于骨髓移植后第5天开始升高,第15天达到高峰。骨髓移植第5、10天小鼠肝脏以充血、水肿变化为主,肝组织存在炎症细胞浸润;第15、20天小鼠肝脏充血、水肿及坏死减轻,以肝脏纤维化为主要表现,炎症浸润明显。单纯照射组小鼠照射后10d内全部死亡,肝脏充血、水肿严重。与NS组小鼠相比较,单纯骨髓移植组小鼠TNF-a、IL-6和MCP-1浓度明显升高。结论成功建立异基因骨髓移植后肝静脉闭塞病模型。肝静脉闭塞病的机制与全身照射后造成的肝脏内皮损伤、炎症细胞浸润及移植后细胞因子的变化密切相关。 | 孙海英 徐开林 安立才 齐昆明 潘彬 房婷 化静 刘迷迷 曾令宇 | 2013 | 中华器官移植杂志2013，34，1： | 1 |
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