TY - JOUR
T1 - Expression of peroxisome proliferator-activated receptor (PPAR)-α and PPAR-γ in the lung tissue of obese mice and the effect of rosiglitazone on proinflammatory cytokine expressions in the lung tissue
AU - Ryu, Seunglok
AU - Shim, Jae Won
AU - Kim, Duk Soo
AU - Jung, Hye Lim
AU - Park, Moon Soo
AU - Park, Soo Hee
AU - Lee, Jinmi
AU - Lee, Won Young
AU - Shim, Jung Yeon
PY - 2013
Y1 - 2013
N2 - Purpose: We investigated the mRNA levels of peroxisome proliferator-activated receptor (PPAR)-α, PPAR-γ, adipokines, and cytokines in the lung tissue of lean and obese mice with and without ovalbumin (OVA) challenge, and the effect of rosiglitazone, a PPAR-γ agonist. Methods: We developed 6 mouse models: OVA-challenged lean mice with and without rosiglitazone; obese mice with and without rosiglitazone; and OVA-challenged obese mice with and without rosiglitazone. We performed real-time polymerase chain reaction for leptin, leptin receptor, adiponectin, vascular endothelial growth factor (VEGF), tumor necrosis factor (TNF)-α, transforming growth factor (TGF)-β, PPAR-α and PPAR-γ from the lung tissue and determined the cell counts and cytokine levels in the bronchoalveolar lavage fluid. Results: Mice with OVA challenge showed airway hyperresponsiveness. The lung mRNA levels of PPARα and PPAR-γ increased significantly in obese mice with OVA challenge compared to that in other types of mice and decreased after rosiglitazone administeration. Leptin and leptin receptor expression increased in obese mice with and without OVA challenge and decreased following rosiglitazone treatment. Adiponectin mRNA level increased in lean mice with OVA challenge. Lung VEGF, TNF-α, and TGF-β mRNA levels increased in obese mice with and without OVA challenge compared to that in the control mice. However, rosiglitazone reduced only TGF-β expression in obese mice, and even augmented VEGF expression in all types of mice. Rosiglitazone treatment did not reduce airway responsiveness, but increased neutrophils and macrophages in the bronchoalveolar lavage fluid. Conclusion: PPAR-α and PPAR-γ expressions were upregulated in the lung tissue of OVA-challenged obese mice however, rosiglitazone treatment did not downregulate airway inflammation in these mice.
AB - Purpose: We investigated the mRNA levels of peroxisome proliferator-activated receptor (PPAR)-α, PPAR-γ, adipokines, and cytokines in the lung tissue of lean and obese mice with and without ovalbumin (OVA) challenge, and the effect of rosiglitazone, a PPAR-γ agonist. Methods: We developed 6 mouse models: OVA-challenged lean mice with and without rosiglitazone; obese mice with and without rosiglitazone; and OVA-challenged obese mice with and without rosiglitazone. We performed real-time polymerase chain reaction for leptin, leptin receptor, adiponectin, vascular endothelial growth factor (VEGF), tumor necrosis factor (TNF)-α, transforming growth factor (TGF)-β, PPAR-α and PPAR-γ from the lung tissue and determined the cell counts and cytokine levels in the bronchoalveolar lavage fluid. Results: Mice with OVA challenge showed airway hyperresponsiveness. The lung mRNA levels of PPARα and PPAR-γ increased significantly in obese mice with OVA challenge compared to that in other types of mice and decreased after rosiglitazone administeration. Leptin and leptin receptor expression increased in obese mice with and without OVA challenge and decreased following rosiglitazone treatment. Adiponectin mRNA level increased in lean mice with OVA challenge. Lung VEGF, TNF-α, and TGF-β mRNA levels increased in obese mice with and without OVA challenge compared to that in the control mice. However, rosiglitazone reduced only TGF-β expression in obese mice, and even augmented VEGF expression in all types of mice. Rosiglitazone treatment did not reduce airway responsiveness, but increased neutrophils and macrophages in the bronchoalveolar lavage fluid. Conclusion: PPAR-α and PPAR-γ expressions were upregulated in the lung tissue of OVA-challenged obese mice however, rosiglitazone treatment did not downregulate airway inflammation in these mice.
KW - Obesity
KW - Peroxisome proliferator-activated receptors
KW - Transforming growth factor-beta
KW - Tumor necrosis factor-alpha
KW - Vascularendothelial growth factor
UR - https://www.scopus.com/pages/publications/84876498250
U2 - 10.3345/kjp.2013.56.4.151
DO - 10.3345/kjp.2013.56.4.151
M3 - Article
AN - SCOPUS:84876498250
SN - 1738-1061
VL - 56
SP - 151
EP - 158
JO - Korean Journal of Pediatrics
JF - Korean Journal of Pediatrics
IS - 4
ER -