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Gastroenterology:急性胰腺炎发病与特殊基因有关

  1. Gastroenterology
  2. 胰腺炎

来源:新华网 2012-11-18 10:35

日本秋田大学研究人员在美国医学杂志《胃肠病学》9月号上发表论文说,他们在世界上首次确认与急性胰腺炎发病有关的基因。 急性胰腺炎很容易发展成为重症,会引起多脏器衰竭和败血症,死亡率达到60%。在急性胰腺炎发病过程中,存在一种自我消化的现象,即胰液中消化酶的功能异常升高,损伤患者自身的胰腺组织。 秋田大学大西洋英和真嶋浩聪领导的研究小组,对“干扰素抑制因子2”的编码基因进行了研究。

日本秋田大学研究人员在美国医学杂志《胃肠病学》9月号上发表论文说,他们在世界上首次确认与急性胰腺炎发病有关的基因。

急性胰腺炎很容易发展成为重症,会引起多脏器衰竭和败血症,死亡率达到60%。在急性胰腺炎发病过程中,存在一种自我消化的现象,即胰液中消化酶的功能异常升高,损伤患者自身的胰腺组织。

秋田大学大西洋英和真嶋浩聪领导的研究小组,对“干扰素抑制因子2”的编码基因进行了研究。他们发现,这一基因存在缺陷的实验鼠胰腺功能存在异常。具体表现是,实验鼠胰腺原来向外部分泌的消化酶无法排出,导致胰腺部位出现剧痛,这与急性胰腺炎的症状相同。

大西洋英指出,此次发现有助于开发出治疗急性胰腺炎的新方法。(生物谷 Bioon.com)

Interferon Regulatory Factor-2 Regulates Exocytosis Mechanisms Mediated by SNAREs in Pancreatic Acinar Cells

Hirosato Mashima, Taku Sato, Yasuo Horie, Yasuo Horie

Background & Aims Pancreatic acinar cells are used to study regulated exocytosis. We investigated the role of interferon regulatory factor-2 (IRF2) in exocytosis in pancreatic acinar cells. Methods Pancreas tissues from Irf2+/+, Irf2+/−, and Irf2−/− mice were examined by microscopy, immunohistochemical, and immunoblot analyses; amylase secretion was quantified. We also compared salivary glands and pancreatic islets of Irf2−/− mice with those of Irf2+/− mice. To examine the effects of increased signaling by type I interferons, we studied pancreatic acini from Irf2−/−Ifnar1−/− mice. The effect of IRF2 on amylase secretion was studied using an acinar cell line and a retroviral system. We studied expression of IRF2 in wild-type mice with cerulein-induced pancreatitis and changes in pancreatic tissue of Irf2−/− mice, compared with those of Irf2+/− mice. Results Irf2−/− pancreas was white and opaque; numerous and wide-spread zymogen granules were observed throughout the cytoplasm, along with lack of fusion between zymogen granules and the apical membrane, lack of secretagogue-stimulated amylase secretion, and low serum levels of amylase and elastase-1, indicating altered regulation of exocytosis. The expression pattern of soluble N-ethylmaleimide-sensitive factor attachment protein receptors changed significantly, specifically in pancreatic acini, and was not rescued by disruption of type I interferon signaling. Down-regulation of IRF2 decreased amylase secretion in an acinar cell line. In mice with pancreatitis, levels of IRF2 were reduced. Irf2−/− acini were partially resistant to induction of pancreatitis. Conclusions IRF2 regulates exocytosis in pancreatic acinar cells; defects in this process might be involved in the early phases of acute pancreatitis.

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