Abstract
It has been reported that DOK3 protein negatively regulates LPS responses and endotoxin tolerance in mice. However, the role of DOK3 in the development of acute respiratory distress syndrome (ARDS) remains unknown. In this study, we showed that DOK3 is degraded in the lung tissues of LPS-induced ARDS. Through lentivirus transduction containing DOK3(K27R) via the intranasal route, we created a mice model, in which DOK3 maintains stable expression. We found that the forced DOK3 expression significantly attenuated LPS-induced pulmonary histological alterations, inflammatory cells infiltration, lung edema, as well as the generation of inflammatory cytokines TNFα, IL- 1β and IL-6 in BALF of LPS-induced ARDS mice. In addition, DOK3 expression apparently suppressed LPS-induced NF-κB and ERK activation. These data suggested that DOK3 expression negatively regulates the development of LPS-induced ARDS in mice.
Keywords: ARDS, DOK3, Lentivirus, LPS, Degradation, Expression.
Current Gene Therapy
Title:DOK3 Degradation is Required for the Development of LPS-induced ARDS in Mice
Volume: 16 Issue: 4
Author(s): Ning Liu, Xiaofeng Liu, Xiaoou Li, Kaifang Duan, Yuming Deng, Xiuyan Yu and Qisheng Peng
Affiliation:
Keywords: ARDS, DOK3, Lentivirus, LPS, Degradation, Expression.
Abstract: It has been reported that DOK3 protein negatively regulates LPS responses and endotoxin tolerance in mice. However, the role of DOK3 in the development of acute respiratory distress syndrome (ARDS) remains unknown. In this study, we showed that DOK3 is degraded in the lung tissues of LPS-induced ARDS. Through lentivirus transduction containing DOK3(K27R) via the intranasal route, we created a mice model, in which DOK3 maintains stable expression. We found that the forced DOK3 expression significantly attenuated LPS-induced pulmonary histological alterations, inflammatory cells infiltration, lung edema, as well as the generation of inflammatory cytokines TNFα, IL- 1β and IL-6 in BALF of LPS-induced ARDS mice. In addition, DOK3 expression apparently suppressed LPS-induced NF-κB and ERK activation. These data suggested that DOK3 expression negatively regulates the development of LPS-induced ARDS in mice.
Export Options
About this article
Cite this article as:
Liu Ning, Liu Xiaofeng, Li Xiaoou, Duan Kaifang, Deng Yuming, Yu Xiuyan and Peng Qisheng, DOK3 Degradation is Required for the Development of LPS-induced ARDS in Mice, Current Gene Therapy 2016; 16 (4) . https://dx.doi.org/10.2174/1566523216666161103142342
DOI https://dx.doi.org/10.2174/1566523216666161103142342 |
Print ISSN 1566-5232 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5631 |
Call for Papers in Thematic Issues
Programmed Cell Death Genes in Oncology: Pioneering Therapeutic and Diagnostic Frontiers (BMS-CGT-2024-HT-45)
Programmed Cell Death (PCD) is recognized as a pivotal biological mechanism with far-reaching effects in the realm of cancer therapy. This complex process encompasses a variety of cell death modalities, including apoptosis, autophagic cell death, pyroptosis, and ferroptosis, each of which contributes to the intricate landscape of cancer development and ...read more
Related Journals
- Author Guidelines
- Graphical Abstracts
- Fabricating and Stating False Information
- Research Misconduct
- Post Publication Discussions and Corrections
- Publishing Ethics and Rectitude
- Increase Visibility of Your Article
- Archiving Policies
- Peer Review Workflow
- Order Your Article Before Print
- Promote Your Article
- Manuscript Transfer Facility
- Editorial Policies
- Allegations from Whistleblowers
- Announcements
Related Articles
-
Telomere Shortening Is a Sole Mechanism of Aging in Mammals
Current Aging Science Natural Oils as Skin Permeation Enhancers for Transdermal Delivery of Olanzapine: In Vitro and In Vivo Evaluation
Current Drug Delivery Neurotrophins in the Lower Urinary Tract: Becoming of Age
Current Neuropharmacology C-reactive Protein, Infection, and Outcome After Acute Ischemic Stroke: A Registry and Systematic Review
Current Neurovascular Research Natural Killer T Cells as Targets for Therapeutic Intervention in Autoimmune Diseases
Current Pharmaceutical Design CETUXIMAB: From Bench to Bedside
Current Cancer Drug Targets Computational Drug Repositioning: A Lateral Approach to Traditional Drug Discovery?
Current Topics in Medicinal Chemistry Synthesis of Novel Heterocyclic Prostaglandin Analogues
Letters in Organic Chemistry A Critical Analysis of New Molecular Targets and Strategies for Drug Developments in Alzheimers Disease
Current Drug Targets Editorial
Current Enzyme Inhibition The HOX Gene Network as a Potential Target for Cancer Therapy
Current Cancer Therapy Reviews Targeting Heat Shock Proteins 70/90 and Proteasome for Cancer Therapy
Current Medicinal Chemistry Immunoglobulin Free Light Chains in Immune Responses
Current Immunology Reviews (Discontinued) Scaffold-based Drug Delivery for Cartilage Tissue Regeneration
Current Pharmaceutical Design Nontraditional Cardiovascular Risk Factors in Pediatric Type 1 Diabetes
Current Diabetes Reviews The Role of An Experimental Model of Atherosclerosis: apoE-knockout Mice in Developing New Drugs against Atherogenesis
Current Pharmaceutical Biotechnology Platelets in Angiogenesis
Current Vascular Pharmacology MicroRNAs: An Apparent Switch for High-Altitude Pulmonary Edema
MicroRNA Therapeutic Approaches for Reducing C-Reactive Protein (CRP) Levels and the Associated Cardiovascular Risk
Current Chemical Biology Advances in Molecular Therapeutic Approaches to Patients with Malignant Gliomas
Current Signal Transduction Therapy