Wednesday, 14 October 2015
Hall D1 Foyer (Floor 3) (Coex Convention Center)
Jin-Young Lee, MD, PhD
,
Health Promotion Center, Samsung Medical Center, Seoul, South Korea
Mi-Jung Oh, MD, PhD
,
Bundang Jesaeng Hospital, BUNDANG, South Korea
Young Hee Lim, MD, PhD
,
Ansan Sarang General Hospital, Ansan, South Korea
Kyoung Won Ha, MD
,
Seoul Samsung Medical Clinic, Incheon, South Korea
Jae-Won Paeng
,
Samsung Biomedical Research Institute, Seoul, South Korea
Mi-Jin Jang
,
Samsung Biomedical Research Institute, Seoul, South Korea
Sehyo Yune, MD
,
Department of Medicine, Samsung Medical Center, Seoul, South Korea
Byung-Jae Lee, MD, PhD
,
Samsung Medical Center, Seoul, South Korea
Dong-Chull Choi, MD, PhD
,
Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, South Korea
Background: S-nitrosothiols (SNOs) are potent endogenous bronchodilators. Genetic ablation of S-nitrosoglutathione reductase (GSNOR), which catalyzes the metabolism of SNOs, results in protection from airway hyperresponsiveness (AHR) in mouse. This study was performed to know whether activity of GSNOR of mice may explain the strain differences in AHR.
Methods: Three different strains of mice - A/J, BALB/c, and C57BL/6 – were untreated (control, each n=5) or were sensitized and challenged with ovalbumin (asthma model, each n=5). AHR was measured using methacholine and activity of GSNOR was measured in whole lung lysate.
Results: Persistent increase of AHR was observed in A/J compared to BALB/c or C57BL/6 control mice. GSNOR activity was significantly higher in A/J than BALB/c or C57BL/6 control mice (596.8±217.5, 400.0±184.8, 263.1±121.7; au, nmol/min/mg, p <0.05). In asthma model, AHR were also increased in AJ mice compared to other strains, and GSNOR activity was higher than BALB/c or C57BL/6 asthma model mice (749.7±192.5, 466.3±218.1, 474.4±24.0; au, nmol/min/mg).
Conclusion: GSNOR activity may contribute to the difference of AHR between mouse strains.
