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Decrease of intracellular chloride concentration promotes endothelial cell inflammation by activating nuclear

Hui Yang1, Lin-Yan Huang, De-Yi Zeng

  • 1Department of Pharmacology, Cardiac and Cerebral Vascular Research Center, Zhongshan School of Medicine, Sun Yat-Sen University, 74 Zhongshan 2 Rd, Guangzhou 510080, China.

Hypertension (Dallas, Tex. : 1979)
|September 26, 2012
PubMed
Summary
This summary is machine-generated.

Reduced intracellular chloride via ClC-3 channel activity enhances nuclear factor (NF)-κB activation and vascular inflammation. Inhibiting ClC-3 may offer a new therapeutic strategy for inflammatory diseases.

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Area of Science:

  • Molecular Biology
  • Cell Biology
  • Immunology

Background:

  • Nuclear factor (NF)-κB signaling is crucial in regulating inflammatory responses.
  • The role of the ClC-3 channel/antiporter in NF-κB activation is not fully understood.
  • Intracellular chloride concentration ([Cl(-)](i)) is a potential mediator of ClC-3's effect on NF-κB.

Purpose of the Study:

  • To elucidate the mechanism by which ClC-3 modulates NF-κB signaling in endothelial cells.
  • To investigate the role of intracellular chloride concentration in ClC-3's regulation of NF-κB.
  • To evaluate the therapeutic potential of targeting ClC-3 in inflammatory diseases.

Main Methods:

  • Utilized human umbilical vein endothelial cells and mouse aortic endothelial cells.
  • Manipulated intracellular chloride concentration and ClC-3 expression (knockdown/knockout).
  • Assessed NF-κB activation, inflammatory marker expression (ICAM-1, VCAM-1), monocyte adhesion, and inflammatory infiltration in vivo.

Main Results:

  • Reduced [Cl(-)](i) potentiated TNFα-induced ICAM-1/VCAM-1 expression and monocyte adhesion.
  • ClC-3 knockdown/knockout inhibited TNFα-induced NF-κB activation and inflammatory responses.
  • ClC-3 knockout mice exhibited attenuated TNFα-induced vascular inflammation and neutrophil infiltration.

Conclusions:

  • ClC-3-dependent chloride efflux, leading to decreased [Cl(-)](i), promotes NF-κB activation.
  • This mechanism potentiates TNFα-induced vascular inflammation.
  • Inhibition of ClC-3 or modulation of intracellular chloride presents a novel therapeutic avenue for inflammatory diseases.