Presentation: Regulatory Role of Progranulin in Cigarette Smoke Extract–Exposed Lung Epithelial Cells. ( World Allergy Congress)

Thursday, 15 October 2015

Hall D1 Foyer (Floor 3) (Coex Convention Center)

Kyoung Young Lee, BS , Asan Institute for Life Sciences, Seoul, South Korea

Sunjoo Park, PhD , Asan Institute for Life Sciences, Seoul, South Korea

Gyong Hwa Hong, BS , Asan Institute for Life Sciences, Seoul, South Korea

So Young Park, MD , Department of Allergy and Clinical Immunology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, South Korea

Keun Ai Moon, MS , Asan Institute for Life Sciences, Seoul, South Korea

Eun Hee Ha, BS , Asan Institute for Life Sciences, Seoul, South Korea

Hyouk-Soo Kwon, MD, PhD , Department of Allergy and Clinical Immunology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, South Korea

Tae-Bum Kim, MD, PhD , Department of Allergy and Clinical Immunology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, South Korea

Hee-Bom Moon, MD, PhD , Department of Allergy and Clinical Immunology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, South Korea

You Sook Cho, MD, PhD , Department of Allergy and Clinical Immunology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, South Korea

Background

Emphysema is characterized by irreversible destruction of alveolar walls with enlargement of distal airspaces. Cigarette smoke (CS) is considered as a main causative factor for the development of emphysematous change in chronic obstructive airway disease. Progranulin (PGRN) has been reported to be induced in response to various stimuli including CS. Recently, PGRN is reported to participate in apoptosis process that is well known cause of alveolar wall destruction. However, the role of PGRN in emphysema is currently unknown.

Aim

We tested if there is a regulatory role of PGRN in human alveolar epithelial cells exposed to CSE.

Methods

Both protein and mRNA expression levels of PGRN were measured in A549 cells after exposure to cigarette smoke extract (CSE). The effect of PGRN on CSE-mediated apoptosis was determined by using flowcytometry analysis with annexin V and PI staining in PGRN-silencing A549 cells.

Results

PGRN expression was increased in A549 cells treated with CSE. A significant increase of active caspase-3 and active PARP expression was detected in PGRN-silencing A549 cells after CSE exposure. Frequency of apoptotic cell death was also significantly increased in PGRN knock-down cells.

Conclusion

PGRN plays a potential role in the development of emphysema probably by preventing apoptosis of alveolar cells.

2149 Regulatory Role of Progranulin in Cigarette Smoke Extract–Exposed Lung Epithelial Cells.