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NAIP expression increases in a rat model of liver mass restoration
Journal of Molecular Histology ( IF 2.9 ) Pub Date : 2020-11-25 , DOI: 10.1007/s10735-020-09928-y
Julio Plaza-Díaz 1, 2, 3, 4 , Ana I Álvarez-Mercado 1, 2, 3 , Cándido Robles-Sánchez 1, 2 , Miguel Navarro-Oliveros 3 , Virginia Morón-Calvente 5 , Sofía Toribio-Castelló 6 , María José Sáez-Lara 2, 3, 7 , Alex MacKenzie 4, 8 , Luis Fontana 1, 2, 3 , Francisco Abadía-Molina 2, 9
Affiliation  

The neuronal apoptosis inhibitory protein (NAIP) is a constituent of the NLRC4 inflammasome, which plays a key role in innate immunity, and an antiapoptotic protein. Recently, we reported the previously undescribed role of NAIP in cell division. The liver is one of the body’s most actively regenerative organs. Given the novel mitotic role of NAIP, we examined its expression in hepatic mass restoration. The major liver lobe of Wistar rats was removed, and samples from both newly formed liver tissue, assessed by positive Ki67 immunostaining, and the remnant, intact liver lobes from hepatectomized rats were taken 3 and 7 days after surgery. Naip5 and Naip6 mRNA levels were significantly higher in regenerating hepatic tissue than in intact liver lobe tissue, and this increase was also observed at the protein level. Naip5 and Naip6 mRNA in situ hybridization showed that this increase occurred in the hepatic parenchyma. The histology of the regenerated liver tissue was normal, with the exception of a noticeable deficiency of hepatic lobule central veins. The results of this study suggest the involvement of NAIP in liver mass restoration following partial hepatectomy.



中文翻译:


肝脏质量恢复大鼠模型中 NAIP 表达增加



神经元凋亡抑制蛋白 (NAIP) 是 NLRC4 炎症小体的组成部分,在先天免疫中发挥着关键作用,也是一种抗凋亡蛋白。最近,我们报道了 NAIP 在细胞分裂中先前未描述的作用。肝脏是人体再生最活跃的器官之一。鉴于 NAIP 的新有丝分裂作用,我们检查了其在肝质量恢复中的表达。切除 Wistar 大鼠的主要肝叶,并在手术后 3 天和 7 天从新形成的肝组织中采集样本(通过阳性 Ki67 免疫染色进行评估),并从肝切除大鼠中采集剩余的完整肝叶。再生肝组织中的Naip5Naip6 mRNA 水平显着高于完整肝叶组织,并且在蛋白质水平上也观察到这种增加。 Naip5Naip6 mRNA原位杂交显示这种增加发生在肝实质中。再生肝组织的组织学正常,但肝小叶中央静脉明显缺乏。这项研究的结果表明 NAIP 参与部分肝切除术后肝脏质量的恢复。

更新日期:2020-11-25
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