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2017 ; 18
(1
): 79
Nephropedia Template TP
Kainuma K
; Kobayashi T
; D'Alessandro-Gabazza CN
; Toda M
; Yasuma T
; Nishihama K
; Fujimoto H
; Kuwabara Y
; Hosoki K
; Nagao M
; Fujisawa T
; Gabazza EC
Respir Res
2017[May]; 18
(1
): 79
PMID28464879
show ga
BACKGROUND: Epithelial-mesenchymal transition is currently recognized as an
important mechanism for the increased number of myofibroblasts in cancer and
fibrotic diseases. We have already reported that epithelial-mesenchymal
transition is involved in airway remodeling induced by eosinophils. Procaterol is
a selective and full ?(2) adrenergic agonist that is used as a rescue of
asthmatic attack inhaler form and orally as a controller. In this study, we
evaluated whether procaterol can suppress epithelial-mesenchymal transition of
airway epithelial cells induced by eosinophils. METHODS: Epithelial-mesenchymal
transition was assessed using a co-culture system of human bronchial epithelial
cells and primary human eosinophils or an eosinophilic leukemia cell line.
RESULTS: Procaterol significantly inhibited co-culture associated morphological
changes of bronchial epithelial cells, decreased the expression of vimentin, and
increased the expression of E-cadherin compared to control. Butoxamine, a
specific ?(2)-adrenergic antagonist, significantly blocked changes induced by
procaterol. In addition, procaterol inhibited the expression of adhesion
molecules induced during the interaction between eosinophils and bronchial
epithelial cells, suggesting the involvement of adhesion molecules in the process
of epithelial-mesenchymal transition. Forskolin, a cyclic adenosine
monophosphate-promoting agent, exhibits similar inhibitory activity of
procaterol. CONCLUSIONS: Overall, these observations support the beneficial
effect of procaterol on airway remodeling frequently associated with chronic
obstructive pulmonary diseases.
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