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本文引用的文献

1
Anionic poly(amino acid)s dissolve F-actin and DNA bundles, enhance DNase activity, and reduce the viscosity of cystic fibrosis sputum.阴离子聚氨基酸可溶解F-肌动蛋白和DNA束,增强脱氧核糖核酸酶活性,并降低囊性纤维化痰液的黏度。
Am J Physiol Lung Cell Mol Physiol. 2005 Oct;289(4):L599-605. doi: 10.1152/ajplung.00061.2005. Epub 2005 Jun 17.
2
hCLCA1 and mCLCA3 are secreted non-integral membrane proteins and therefore are not ion channels.人氯离子通道辅助蛋白1(hCLCA1)和小鼠氯离子通道辅助蛋白3(mCLCA3)是分泌型非整合膜蛋白,因此不是离子通道。
J Biol Chem. 2005 Jul 22;280(29):27205-12. doi: 10.1074/jbc.M504654200. Epub 2005 May 25.
3
Increased expression of the calcium-activated chloride channel hCLCA1 in airways of patients with obstructive chronic bronchitis.钙激活氯离子通道hCLCA1在阻塞性慢性支气管炎患者气道中的表达增加。
Can Respir J. 2005 Apr;12(3):143-6. doi: 10.1155/2005/531432.
4
Niflumic acid and MSI-2216 reduce TNF-alpha-induced mucin expression in human airway mucosa.尼氟灭酸和MSI-2216可降低肿瘤坏死因子-α诱导的人气道黏膜黏蛋白表达。
J Allergy Clin Immunol. 2005 Feb;115(2):266-71. doi: 10.1016/j.jaci.2004.09.039.
5
Dual oxidase 1-dependent MUC5AC mucin expression in cultured human airway epithelial cells.双氧化酶1依赖性MUC5AC粘蛋白在培养的人气道上皮细胞中的表达
Proc Natl Acad Sci U S A. 2005 Jan 18;102(3):767-72. doi: 10.1073/pnas.0408932102. Epub 2005 Jan 7.
6
Expression of HCLCA1 in cystic fibrosis lungs is associated with mucus overproduction.HCLCA1在囊性纤维化肺中的表达与黏液过度产生有关。
Eur Respir J. 2004 Jun;23(6):846-50. doi: 10.1183/09031936.04.00096504.
7
Cigarette smoke induces MUC5AC mucin overproduction via tumor necrosis factor-alpha-converting enzyme in human airway epithelial (NCI-H292) cells.香烟烟雾通过肿瘤坏死因子-α转化酶在人气道上皮(NCI-H292)细胞中诱导MUC5AC粘蛋白过度产生。
Am J Physiol Lung Cell Mol Physiol. 2004 Aug;287(2):L420-7. doi: 10.1152/ajplung.00019.2004. Epub 2004 Apr 30.
8
MUC5AC and MUC5B Mucins Are Decreased in Cystic Fibrosis Airway Secretions.黏蛋白MUC5AC和MUC5B在囊性纤维化气道分泌物中减少。
Am J Respir Cell Mol Biol. 2004 Jul;31(1):86-91. doi: 10.1165/rcmb.2003-0345OC. Epub 2004 Feb 26.
9
A MARCKS-related peptide blocks mucus hypersecretion in a mouse model of asthma.一种与MARCKS相关的肽可阻断哮喘小鼠模型中的黏液分泌过多。
Nat Med. 2004 Feb;10(2):193-6. doi: 10.1038/nm983. Epub 2004 Jan 11.
10
Molecular cloning, genomic structure, and expression analysis of MUC20, a novel mucin protein, up-regulated in injured kidney.新型黏蛋白MUC20在损伤肾脏中上调,其分子克隆、基因组结构及表达分析
J Biol Chem. 2004 Jan 16;279(3):1968-79. doi: 10.1074/jbc.M304558200. Epub 2003 Oct 17.

慢性炎症性肺病中的粘蛋白过度产生。

Mucin overproduction in chronic inflammatory lung disease.

作者信息

Hauber Hans-Peter, Foley Susan C, Hamid Qutayba

机构信息

McGill University, Montreal, Quebec.

出版信息

Can Respir J. 2006 Sep;13(6):327-35. doi: 10.1155/2006/901417.

DOI:10.1155/2006/901417
PMID:16983448
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2683320/
Abstract

Mucus overproduction and hypersecretion are commonly observed in chronic inflammatory lung disease. Mucins are gel-forming glycoproteins that can be stimulated by a variety of mediators. The present review addresses the mechanisms involved in the upregulation of secreted mucins. Mucin induction by neutrophil elastase, bacteria, cytokines, growth factors, smoke and cystic fibrosis transmembrane conductance regulator malfunction are also discussed.

摘要

在慢性炎症性肺病中,通常会观察到黏液过度产生和分泌过多的现象。黏蛋白是可形成凝胶的糖蛋白,可被多种介质刺激。本综述探讨了分泌型黏蛋白上调所涉及的机制。还讨论了中性粒细胞弹性蛋白酶、细菌、细胞因子、生长因子、烟雾和囊性纤维化跨膜传导调节因子功能障碍对黏蛋白的诱导作用。