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Suppression of vascular permeability and inflammation by targeting of the transcription factor c-Jun
Roger G Fahmy1, Alla Waldman, Guishui Zhang
1Centre for Vascular Research, University of New South Wales, and Department of Haematology, The Prince of Wales Hospital, Sydney NSW 2031, Australia.
Abstract:
Conventional anti-inflammatory strategies induce multiple side effects, highlighting the need for novel targeted therapies. Here we show that knockdown of the basic-region leucine zipper protein, c-Jun, by a catalytic DNA molecule, Dz13, suppresses vascular permeability and transendothelial emigration of leukocytes in murine models of vascular permeability, inflammation, acute inflammation and rheumatoid arthritis. Treatment with Dz13 reduced vascular permeability due to cutaneous anaphylactic challenge or VEGF administration in mice. Dz13 also abrogated monocyte-endothelial cell adhesion in vitro and abolished leukocyte rolling, adhesion and extravasation in a rat model of inflammation. Dz13 suppressed neutrophil infiltration in the lungs of mice challenged with endotoxin, a model of acute inflammation. Finally, Dz13 reduced joint swelling, inflammatory cell infiltration and bone erosion in a mouse model of rheumatoid arthritis. Mechanistic studies showed that Dz13 blocks cytokine-inducible endothelial c-Jun, E-selectin, ICAM-1, VCAM-1 and VE-cadherin expression but has no effect on JAM-1, PECAM-1, p-JNK-1 or c-Fos. These findings implicate c-Jun as a useful target for anti-inflammatory therapies.
Insights
Targeting c-Jun with DNAzyme Dz13 effectively reduces vascular permeability and leukocyte migration. This novel approach shows promise for treating inflammatory diseases like rheumatoid arthritis with fewer side effects.
Area of Science:
- Molecular Biology
- Immunology
- Pharmacology
Background:
- Conventional anti-inflammatory drugs cause side effects, necessitating targeted therapies.
- Vascular permeability and leukocyte emigration are key processes in inflammation.
Purpose of the Study:
- To investigate the efficacy of DNAzyme Dz13 in suppressing inflammation by targeting c-Jun.
- To evaluate Dz13 as a novel therapeutic agent for inflammatory conditions.
Main Methods:
- Utilized murine models for vascular permeability, inflammation, acute inflammation, and rheumatoid arthritis.
- Administered Dz13 to assess its impact on vascular permeability, leukocyte adhesion, and infiltration.
- Conducted mechanistic studies to identify molecular targets of Dz13.
Main Results:
- Dz13 significantly reduced vascular permeability induced by anaphylactic challenge or VEGF.
- Dz13 inhibited leukocyte rolling, adhesion, and extravasation in inflammatory models.
- Dz13 suppressed neutrophil infiltration and attenuated joint swelling and bone erosion in rheumatoid arthritis models.
Conclusions:
- Targeting c-Jun with Dz13 is a viable strategy for developing novel anti-inflammatory therapies.
- Dz13 effectively blocks key inflammatory pathways, including endothelial adhesion molecule expression.
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