Scientific Program

Conference Series Ltd invites all the participants across the globe to attend 4thInternational Conference on Chronic Obstructive Pulmonary Disease Osaka,Japan.

Day 1 :

OMICS International COPD 2017 International Conference Keynote Speaker Yong-Xiao Wang photo
Biography:

Dr. Yong-Xiao Wang has been a Full Professor in Albany Medical College (USA) since 2006. Dr. Wang has had extensive research experience in basic, translational and drug research concerning pulmonary hypertension, asthma, chronic obstructive pulmonary disease, diabetes, and cardiac arrhythmia for over 30 years. As the Principal Investigator, he has/had numerous NIH R01 research awards, AHA Established Investigator Award, and various other grants, for which he often holds/held 2 – 3 NIH R01 grants with other awards each year. As the corresponding author, first author and key contributor, he has had numerous publications in highly peer-reviewed journals including Antioxid Redox Signal (impact factor: 8.209), Proc Natl Acad Sci USA (9.432), Nature (34.480), Circ Res (9.214), etc. Dr. Wang has been the editor of academic books in the field including one entitled by “Redox Signaling in Health and Disease Pulmonary Vasculature” that has been confirmed for publication by Springer (New York). Dr. Wang has also served as the editorial board member and/or section editor for the Clinical and Translational Medicine, Pulmonary Circulation and several other journals.

Abstract:

Statement of the Problem: COPD is the fourth leading cause of mortality in the world and will be the second leading cause of death by 2020. However, the molecular processes for this devastating disease remain largely unknown, and current treatments are limited. Purposes: This study was to test a novel hypothesis that the reciprocal crosstalks between ion channel-mediated calcium signaling and transcriptional factor-dependent inflammatory signaling are essential for COPD. The current study also sought to determine whether specific genetic and pharmacological targets for these signaling molecules would become effective therapeutics for COPD. Methodology: Ion channel expression and activity were assayed using RT-PCR, Western blotting and patch clamp recordings; airway remodeling and hyperresponsiveness examined using in-situ immunohistological staining and both in-vivo and in-vitro muscle contraction measurements; and targeted molecule activities changed using virus-based genetic modifications. Findings: Among 7 known different gene-encoded classic transient receptor potential (TRPC) channel members, only shows the TRPC3 channel a predominant activity and expression in airway smooth muscle cells (ASMCs). This channel is significantly upregulated in COPD patient ASMCs. Mice with nicotine-induced COPD also show largely increased TRPC3 channel expression and activity in ASMCs. In-vivo lentiviral shRNA-mediated TRPC3 channel knockdown abolishes airway remodeling and hyperresponsiveness in COPD. The channel blocker Pyr3 produces similar effects. The TRPC3 channel promoter has binding sites for NFkB, an important inflammatory transcription factor. NFkB expression and activity are increased in COPD ASMCs. Genetic NFkB function gain and loss, respectively, increases and blocks, TRPC3 channel promoter activity and expression. Vise verse, TRPC3 channel gain and loss, downregulates and upregulates, NFkB activity and expression. Conclusion & Significance: Reciprocal crosstalks between TRPC3 channel-mediated calcium signaling and NFkB-dependent inflammatory signaling are essential for airway remodeling and hyperresponsiveness in COPD. Specific lentiviral TRPC3 channel shRNAs and channel blockers may become novel and effective treatments for COPD.

Keynote Forum

Nobuaki Miyahara

Okayama University, Japan

Keynote: Importance of IL-23 to the development of emphysema

Time : 11:00-11:40

OMICS International COPD 2017 International Conference Keynote Speaker Nobuaki Miyahara photo
Biography:

Nobuaki Miyahara graduated from Hiroshima University School of Medicine in 1988. He has completed his PhD in Department of Medicine II, Okayama University School of Medicine in 1994. He had done research on allergic airway inflammation at the National Jewish Health in Denver, CO, USA (Dr. Erwin Gelfand’s Lab) from 2001 to 2008. Currently, he works at Department of Medical Technology, Okayama University Graduate School of Health Sciences, and Department of Allergy and Respiratory Medicine, Okayama University Hospital. His research interest is pathogenesis of COPD and asthma.

Abstract:

Pulmonary emphysema is characterized by alveolar destruction and persistent inflammation of the airways. We have recently reported that IL-17A and Th17 cells play a critical role to the development of porcine pancreatic elastase (PPE)-induced emphysema. Differentiation of Th17 cells is shown to be induced by IL-23. To determine the contribution of IL-23 to the development of pulmonary emphysema a mouse model of PPE-induced emphysema was used in which responses of IL-23p19-deficient (IL-23-/-) and wild type (WT) mice were compared. Intra-tracheal instillation of PPE induced emphysematous changes in the lungs and was associated with increased levels of IL-23 in lung homogenates. Compared to WT mice, IL-23-/- mice developed significantly lower static compliance values and markedly reduced emphysematous changes on histological analyses following PPE-instillation. These changes were associated with lower levels of IL-17A and fewer Th17 cells in the lung. The neutrophilia seen in bronchoalveolar lavage (BAL) fluid of WT mice was attenuated in IL-23-/- mice, and the reduction was associated with decreased levels of KC and MIP-2 in BAL fluid. Treatment with anti-IL-23p40 monoclonal antibody significantly attenuated PPE-induced emphysematous changes in the lungs of WT mice. These data identify the important contributions of IL-23 to the development of elastase-induced pulmonary inflammation and emphysema, mediated through an IL-23-IL-17 pathway. Targeting IL-23 in emphysema may be a potential therapeutic strategy for delaying disease progression.