Pediatr Allergy Respir Dis.
2010 Jun;20(2):100-106.
Induction of Vascular Endothelial Growth Factor Protein by Mycoplasma pneumoniae
- Affiliations
-
- 1Department 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
- 2Department of Microbiology, Kosin University College of Medicine, Busan, Korea.
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.