Induction of Vascular Endothelial Growth Factor Protein by Mycoplasma pneumoniae
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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 μg/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.
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 μg/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.
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