Induction of Vascular Endothelial Growth Factor Protein by Mycoplasma pneumoniae.
- Author:
Kyung Eun LEE
1
;
Jung Yeon HONG
;
Myung Hyun SOHN
;
Kyung Won KIM
;
In Dal PARK
;
Myung Woong CHANG
;
Kyu Earn KIM
Author Information
1. Department of Pediatrics and Institute of Allergy, Brain Korea 21 Project for Medical Science, Severance Medical Research Institute, Yonsei University College of Medicine, Seoul, Korea. kekim@yuhs.ac
- Publication Type:Original Article
- Keywords:
Mycoplasma pneumoniae;
Vascular endothelial growth factor;
Mitogen-activated protein kinase;
Airway epithelial cell
- MeSH:
Angiogenesis Inducing Agents;
Butadienes;
DNA, Complementary;
Enzyme-Linked Immunosorbent Assay;
Epithelial Cells;
Gene Expression;
Hand;
Humans;
Imidazoles;
JNK Mitogen-Activated Protein Kinases;
Mycoplasma;
Mycoplasma pneumoniae;
Nitriles;
Phosphotransferases;
Pneumonia;
Pneumonia, Mycoplasma;
Polymerase Chain Reaction;
Protein Kinases;
Pyridines;
Respiratory System;
RNA;
RNA, Messenger;
Vascular Endothelial Growth Factor A
- From:Pediatric Allergy and Respiratory Disease
2010;20(2):100-106
- CountryRepublic of Korea
- Language:English
-
Abstract:
PURPOSE: Mycoplasma pneumoniae is an extracellular pathogen that attaches to and destroys the ciliated epithelial cells of the respiratory tract. The vascular endothelial growth factor (VEGF) is a critical angiogenic factor that manages the formation and function of vascular networks. Thus, we examined whether M. pneumoniae lysate (MPL) induces VEGF and MPL-induced VEGF expression is regulated by the activation of mitogen-activated protein kinase (MAPK) pathways in airway epithelial cells. METHODS: Cells were treated with MPL in dose and time dependent manners or pretreated with chemical inhibitors of MAPK signaling molecules before the addition of MPL. The supernatants were measured by a specific human VEGF enzyme-linked immunosorbent assay (ELISA). The RNAs were extracted and synthesized into cDNAs for VEGF gene expression by polymerase chain reaction. RESULTS: MPL considerably increased VEGF mRNA 2 hours after treatment, which was gradually reduced thereafter. On the other hand, VEGF protein was continuously amplified for 12 hours after both 5 and 10 microg/mL MPL treatment. Pretreatment with U0126 (a specific extracellular signal-regulated kinase inhibitor) and SB202190 (a specific p38 inhibitor) abolished MPL-stimulated VEGF protein close to basal level (-85%), whereas JNK inhibitor II (a specific c-Jun N-terminal kinase inhibitor) partially decreased VEGF protein (57%). CONCLUSION: We concluded that MPL induces VEGF expression through the activation of MAPK signaling molecules (ERK, p38 and JNK) in airway epithelial cells.
