Suppr超能文献

氯离子通道蛋白2(ClC-2)对肠道屏障功能的调节:基础科学向治疗靶点的转化

ClC-2 regulation of intestinal barrier function: Translation of basic science to therapeutic target.

作者信息

Jin Younggeon, Blikslager Anthony T

机构信息

Department of Clinical Sciences; College of Veterinary Medicine, North Carolina State University ; Raleigh, NC, USA.

出版信息

Tissue Barriers. 2015 Nov 13;3(4):e1105906. doi: 10.1080/21688370.2015.1105906. eCollection 2015 Oct-Dec.

Abstract

The ClC-2 chloride channel is a member of the voltage-gated chloride channel family. ClC-2 is involved in various physiological processes, including fluid transport and secretion, regulation of cell volume and pH, maintaining the membrane potential of the cell, cell-to-cell communication, and tissue homeostasis. Recently, our laboratory has accumulated evidence indicating a critical role of ClC-2 in the regulation of intestinal barrier function by altering inter-epithelial tight junction composition. This review will detail the role of ClC-2 in intestinal barrier function during intestinal disorders, including experimental ischemia/reperfusion injury and dextran sodium sulfate (DSS)-induced inflammatory bowel disease. Details of pharmacological manipulation of ClC-2 via prostone agonists will also be provided in an effort to show the potential therapeutic relevance of ClC-2 regulation, particularly during intestinal barrier disruption.

摘要

氯离子通道蛋白2(ClC-2)是电压门控氯离子通道家族的成员之一。ClC-2参与多种生理过程,包括液体运输与分泌、细胞体积和pH值的调节、维持细胞的膜电位、细胞间通讯以及组织稳态。最近,我们实验室积累了证据,表明ClC-2通过改变上皮细胞间紧密连接的组成,在肠道屏障功能的调节中起关键作用。本综述将详细阐述ClC-2在肠道疾病(包括实验性缺血/再灌注损伤和葡聚糖硫酸钠(DSS)诱导的炎症性肠病)期间肠道屏障功能中的作用。还将提供通过前列腺素激动剂对ClC-2进行药理学调控的细节,以展示ClC-2调节的潜在治疗意义,尤其是在肠道屏障破坏期间。

相似文献

1
ClC-2 regulation of intestinal barrier function: Translation of basic science to therapeutic target.
Tissue Barriers. 2015 Nov 13;3(4):e1105906. doi: 10.1080/21688370.2015.1105906. eCollection 2015 Oct-Dec.
2
Pharmaceutical Activation or Genetic Absence of ClC-2 Alters Tight Junctions During Experimental Colitis.
Inflamm Bowel Dis. 2015 Dec;21(12):2747-57. doi: 10.1097/MIB.0000000000000550.
3
ClC-2 is required for rapid restoration of epithelial tight junctions in ischemic-injured murine jejunum.
Exp Cell Res. 2009 Jan 1;315(1):110-8. doi: 10.1016/j.yexcr.2008.10.001. Epub 2008 Oct 17.
4
ClC-3 chloride channel/antiporter defect contributes to inflammatory bowel disease in humans and mice.
Gut. 2014 Oct;63(10):1587-95. doi: 10.1136/gutjnl-2013-305168. Epub 2014 Jan 17.
5
Recovery of mucosal barrier function in ischemic porcine ileum and colon is stimulated by a novel agonist of the ClC-2 chloride channel, lubiprostone.
Am J Physiol Gastrointest Liver Physiol. 2007 Feb;292(2):G647-56. doi: 10.1152/ajpgi.00183.2006. Epub 2006 Oct 19.
7
ClC-2 regulates mucosal barrier function associated with structural changes to the villus and epithelial tight junction.
Am J Physiol Gastrointest Liver Physiol. 2010 Aug;299(2):G449-56. doi: 10.1152/ajpgi.00520.2009. Epub 2010 May 20.
10

引用本文的文献

1
Chloride channels and mast cell function: pioneering new frontiers in IBD therapy.
Mol Cell Biochem. 2025 Mar 4. doi: 10.1007/s11010-025-05243-w.
2
Living Conditions Alter Ketogenic Diet-induced Metabolic Consequences in Mice through Modulating Gut Microbiota.
Phenomics. 2024 Jun 6;4(4):313-326. doi: 10.1007/s43657-024-00161-1. eCollection 2024 Aug.
3
Inhibition of COX-2 signaling favors E. coli during urinary tract infection.
J Inflamm (Lond). 2023 Sep 11;20(1):30. doi: 10.1186/s12950-023-00356-9.
6
Defining the role of CFTR channel blocker and ClC-2 activator in DNBS induced gastrointestinal inflammation.
Saudi Pharm J. 2021 Apr;29(4):291-304. doi: 10.1016/j.jsps.2021.02.005. Epub 2021 Mar 10.
8
The Regulation of Intestinal Mucosal Barrier by Myosin Light Chain Kinase/Rho Kinases.
Int J Mol Sci. 2020 May 18;21(10):3550. doi: 10.3390/ijms21103550.
9
Lubiprostone protects esophageal mucosa from acid injury in porcine esophagus.
Am J Physiol Gastrointest Liver Physiol. 2020 Apr 1;318(4):G613-G623. doi: 10.1152/ajpgi.00086.2019. Epub 2020 Feb 18.
10
The Integral Role of Tight Junction Proteins in the Repair of Injured Intestinal Epithelium.
Int J Mol Sci. 2020 Feb 1;21(3):972. doi: 10.3390/ijms21030972.

本文引用的文献

1
Pharmaceutical Activation or Genetic Absence of ClC-2 Alters Tight Junctions During Experimental Colitis.
Inflamm Bowel Dis. 2015 Dec;21(12):2747-57. doi: 10.1097/MIB.0000000000000550.
2
Differentiation between human ClC-2 and CFTR Cl- channels with pharmacological agents.
Am J Physiol Cell Physiol. 2014 Sep 1;307(5):C479-92. doi: 10.1152/ajpcell.00077.2014. Epub 2014 Jul 9.
3
Chloride channel ClC-2 is a key factor in the development of DSS-induced murine colitis.
Inflamm Bowel Dis. 2013 Dec;19(13):2867-77. doi: 10.1097/MIB.0b013e3182a82ae9.
5
Lubiprostone Increases Small Intestinal Smooth Muscle Contractions Through a Prostaglandin E Receptor 1 (EP1)-mediated Pathway.
J Neurogastroenterol Motil. 2013 Jul;19(3):312-8. doi: 10.5056/jnm.2013.19.3.312. Epub 2013 Jul 8.
6
Cell biology and physiology of CLC chloride channels and transporters.
Compr Physiol. 2012 Jul;2(3):1701-44. doi: 10.1002/cphy.c110038.
7
Lubiprostone decreases mouse colonic inner mucus layer thickness and alters intestinal microbiota.
Dig Dis Sci. 2013 Mar;58(3):668-77. doi: 10.1007/s10620-012-2509-5. Epub 2013 Jan 18.
8
Dual activation of CFTR and CLCN2 by lubiprostone in murine nasal epithelia.
Am J Physiol Lung Cell Mol Physiol. 2013 Mar 1;304(5):L324-31. doi: 10.1152/ajplung.00277.2012. Epub 2013 Jan 11.
9
Lubiprostone stimulates small intestinal mucin release.
BMC Gastroenterol. 2012 Nov 6;12:156. doi: 10.1186/1471-230X-12-156.
10
Gastro protective properties of the novel prostone SPI-8811 against acid-injured porcine mucosa.
World J Gastroenterol. 2012 Sep 14;18(34):4684-92. doi: 10.3748/wjg.v18.i34.4684.

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验