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特发性乙状结肠巨结肠中Cajal间质细胞的表型改变

Phenotypic alteration of interstitial cells of Cajal in idiopathic sigmoid megacolon.

作者信息

Adachi Yasushi, Ishii Yoshifumi, Yoshimoto Mitsuru, Yoshida Yukinari, Endo Takao, Yamamoto Hiroyuki, Akashi Hirofumi, Imai Kohzoh, Shinomura Yasuhisa, Kato Yasuo

机构信息

Internal Medicine, Sapporo Shirakabadai Hospital, 2-18 Higashi Tsukisamu, Sapporo, 062-0052, Japan.

出版信息

J Gastroenterol. 2008;43(8):626-31. doi: 10.1007/s00535-008-2207-4. Epub 2008 Aug 17.

DOI:10.1007/s00535-008-2207-4
PMID:18709485
Abstract

BACKGROUND

Interstitial cells of Cajal (ICCs) are detected as a pacemaker of gastrointestinal movement and express c-kit and CD34. Recently, ICCs have implicated pathogenesis in several human diseases presenting gastrointestinal motor dysfunction. This study was performed to clarify the role of ICCs in idiopathic sigmoid megacolon using histological and immunohistochemical examinations.

METHODS

Four adult patients with idiopathic sigmoid megacolon and 11 controls were studied. Histology and immunocytochemistry using NSE, S100, c-kit, and CD34 were performed in conjunction with quantitative analysis using the public domain NIH image program.

RESULTS

Little histological change in neuromuscular structures in megacolon was observed. Immunohistochemistry demonstrated remarkable decrease of c-kit expressing ICCs without reduction of CD34 expression in the similar interstitial cell population. This observation was further supported by quantitative assessment using public domain NIH image program.

CONCLUSIONS

A specific downregulation of c-kit in ICCs may be a cause of idiopathic sigmoid megacolon in adults.

摘要

背景

Cajal间质细胞(ICCs)被检测为胃肠运动的起搏器,并表达c-kit和CD34。最近,ICCs与几种表现为胃肠运动功能障碍的人类疾病的发病机制有关。本研究旨在通过组织学和免疫组织化学检查阐明ICCs在特发性乙状结肠巨结肠中的作用。

方法

研究了4例成年特发性乙状结肠巨结肠患者和11例对照。使用NSE、S100、c-kit和CD34进行组织学和免疫细胞化学检查,并结合使用公共领域的NIH图像程序进行定量分析。

结果

在巨结肠中未观察到神经肌肉结构的明显组织学变化。免疫组织化学显示,在相似的间质细胞群体中,表达c-kit的ICCs显著减少,而CD34表达未降低。使用公共领域的NIH图像程序进行的定量评估进一步支持了这一观察结果。

结论

ICCs中c-kit的特异性下调可能是成人特发性乙状结肠巨结肠的一个原因。

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Am J Surg Pathol. 2007 Mar;31(3):460-8. doi: 10.1097/01.pas.0000213371.79300.a8.
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A deficiency of gastric interstitial cells of Cajal accompanied by decreased expression of neuronal nitric oxide synthase and substance P in patients with type 2 diabetes mellitus.2型糖尿病患者胃Cajal间质细胞缺乏,同时神经元型一氧化氮合酶和P物质表达降低。
J Gastroenterol. 2006 Nov;41(11):1076-87. doi: 10.1007/s00535-006-1909-8. Epub 2006 Dec 8.
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The pathogenesis of idiopathic megacolon.
肠道前炎性巨噬细胞诱导 Cajal 间质细胞表型转换。
J Clin Invest. 2020 Dec 1;130(12):6443-6456. doi: 10.1172/JCI126584.
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A Pilot Study of Non-invasive Sacral Nerve Stimulation in Treatment of Constipation in Childhood and Adolescence.一项关于非侵入性骶神经刺激治疗儿童及青少年便秘的初步研究。
Front Pediatr. 2020 Apr 16;8:169. doi: 10.3389/fped.2020.00169. eCollection 2020.
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Chagasic megacolon: enteric neurons and related structures.恰加斯病性巨结肠:肠神经元及相关结构
Histochem Cell Biol. 2014 Sep;142(3):235-44. doi: 10.1007/s00418-014-1250-x. Epub 2014 Jul 25.
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PLoS One. 2014 Apr 15;9(4):e93750. doi: 10.1371/journal.pone.0093750. eCollection 2014.
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Clin Exp Metastasis. 2011 Mar;28(3):291-9. doi: 10.1007/s10585-010-9371-7. Epub 2011 Jan 5.
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特发性巨结肠的发病机制。
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J Physiol. 2006 Nov 1;576(Pt 3):721-6. doi: 10.1113/jphysiol.2006.115279. Epub 2006 Jul 27.
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