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2 results on '"E prostanoid receptor 2"'

1. Microsomal Prostaglandin E Synthase-1 Deficiency Exacerbates Pulmonary Fibrosis Induced by Bleomycin in Mice

Author

Bo Wei, Linhong Cai, Dan Sun, Yanhua Wang, Cairui Wang, Xiaoyu Chai, Feng Xie, Ming Su, Fangrui Ding, Jie Liu, Jichun Yang, Youfei Guan, and Xinmin Liu

Subjects
microsomal prostaglandin E synthase-1, idiopathic pulmonary fibrosis, prostaglandin E2, E prostanoid receptor 2, focal adhesion kinase, Organic chemistry, QD241-441
Abstract

Microsomal prostaglandin E2 synthase-1 (mPGES-1), an inducible enzyme that converts prostaglandin H2 (PGH2) to prostaglandin E2 (PGE2), plays an important role in a variety of diseases. So far, the role of mPGES-1 in idiopathic pulmonary fibrosis (IPF) remained unknown. The current study aimed to investigate the role of mPGES-1 in pulmonary fibrosis induced by bleomycin in mice. We found that mPGES-1 deficient (mPGES-1−/−) mice exhibited more severe fibrotic lesions with a decrease in PGE2 content in lungs after bleomycin treatment when compared with wild type (mPGES-1+/+) mice. The mPGES-1 expression levels and PGE2 content were also decreased in bleomycin-treated mPGES-1+/+ mice compared to saline-treated mPGES-1+/+ mice. Moreover, in both mPGES-1−/− and mPGES-1+/+ mice, bleomycin treatment reduced the expression levels of E prostanoid receptor 2 (EP2) and EP4 receptor in lungs, whereas had little effect on EP1 and EP3. In cultured human lung fibroblast cells (MRC-5), siRNA-mediated knockdown of mPGES-1 augmented transforming growth factor-β1 (TGF-β1)-induced α-smooth muscle actin (α-SMA) protein expression, and the increase was reversed by treatment of PGE2, selective EP2 agonist and focal adhesion kinase (FAK) inhibitor. In conclusion, these findings revealed mPGES-1 exerts an essential effect against pulmonary fibrogenesis via EP2-mediated signaling transduction, and activation of mPGES-1-PGE2-EP2-FAK signaling pathway may represent a new therapeutic strategy for treatment of IPF patients.

Published
2014
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2. Microsomal Prostaglandin E Synthase-1 Deficiency Exacerbates Pulmonary Fibrosis Induced by Bleomycin in Mice

Author

Xinmin Liu, Youfei Guan, Yanhua Wang, Feng Xie, Cairui Wang, Ming Su, Linhong Cai, Bo Wei, Dan Sun, Jichun Yang, Xiaoyu Chai, Fangrui Ding, and Jie Liu

Subjects
Pulmonary Fibrosis, medicine.medical_treatment, Pharmaceutical Science, Analytical Chemistry, Mice, chemistry.chemical_compound, Idiopathic pulmonary fibrosis, Drug Discovery, Pulmonary fibrosis, RNA, Small Interfering, Prostaglandin E2, Lung, Prostaglandin-E Synthases, Mice, Knockout, respiratory system, idiopathic pulmonary fibrosis, Intramolecular Oxidoreductases, Chemistry (miscellaneous), Molecular Medicine, Female, lipids (amino acids, peptides, and proteins), Prostaglandin H2, Signal Transduction, Prostaglandin E, medicine.drug, musculoskeletal diseases, medicine.medical_specialty, Prostaglandin E2 receptor, EP4 Receptor, E prostanoid receptor 2, Biology, Bleomycin, Dinoprostone, Article, microsomal prostaglandin E synthase-1, Cell Line, Transforming Growth Factor beta1, lcsh:QD241-441, lcsh:Organic chemistry, Microsomes, Internal medicine, medicine, Animals, Physical and Theoretical Chemistry, Protein Kinase Inhibitors, prostaglandin E2, Organic Chemistry, focal adhesion kinase, Fibroblasts, Receptors, Prostaglandin E, EP2 Subtype, medicine.disease, Actins, Endocrinology, Gene Expression Regulation, chemistry, Focal Adhesion Kinase 1, Receptors, Prostaglandin E, EP4 Subtype
Abstract

Microsomal prostaglandin E2 synthase-1 (mPGES-1), an inducible enzyme that converts prostaglandin H2 (PGH2) to prostaglandin E2 (PGE2), plays an important role in a variety of diseases. So far, the role of mPGES-1 in idiopathic pulmonary fibrosis (IPF) remained unknown. The current study aimed to investigate the role of mPGES-1 in pulmonary fibrosis induced by bleomycin in mice. We found that mPGES-1 deficient (mPGES-1−/−) mice exhibited more severe fibrotic lesions with a decrease in PGE2 content in lungs after bleomycin treatment when compared with wild type (mPGES-1+/+) mice. The mPGES-1 expression levels and PGE2 content were also decreased in bleomycin-treated mPGES-1+/+ mice compared to saline-treated mPGES-1+/+ mice. Moreover, in both mPGES-1−/− and mPGES-1+/+ mice, bleomycin treatment reduced the expression levels of E prostanoid receptor 2 (EP2) and EP4 receptor in lungs, whereas had little effect on EP1 and EP3. In cultured human lung fibroblast cells (MRC-5), siRNA-mediated knockdown of mPGES-1 augmented transforming growth factor-β1 (TGF-β1)-induced α-smooth muscle actin (α-SMA) protein expression, and the increase was reversed by treatment of PGE2, selective EP2 agonist and focal adhesion kinase (FAK) inhibitor. In conclusion, these findings revealed mPGES-1 exerts an essential effect against pulmonary fibrogenesis via EP2-mediated signaling transduction, and activation of mPGES-1-PGE2-EP2-FAK signaling pathway may represent a new therapeutic strategy for treatment of IPF patients.

Published
2014

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