Airway smooth muscle cells (ASMCs) play a key role in the process of @entity565 airway remodeling. @entity3663 ( @entity3663 ) and transforming growth factor (TGF)-b are potent mitogens for ASMCs proliferation. The study was aimed to determine whether @entity3663 -upregulated @entity1810 -mediated ASMCs proliferation and @entity2509 ( @entity2509 ) was required for such an effect. OVA-sensitized @entity35 were challenged to induce @entity565 . Lung morphology and airway dynamic parameters were monitored. ASMCs from control and @entity565 @entity35 were purified for the measurement of @entity3663 and @entity1810 expression. In vitro experiments were conducted to determine the direct effect of @entity3663 on @entity1810 expression by ASMCs. Finally, @entity5732 , an @entity2509 inhibitor was used to examine the role of @entity2509 pathway in @entity3663 mediated @entity1810 upregulation. We found that both @entity3663 and @entity1810 were upregulated in @entity565 lung tissues. In vitro study on ASMCs further revealed that @entity3663 may render its effect on ASMCs cells through the upregulation of @entity1810 . Data also supported the conclusion that @entity2509 pathway was required, but not sufficient in @entity3663 -induced @entity1810 upregulation. The current study provides new evidence that @entity3663 is involved in the @entity1810 mediated mitogenic effect on ASMCs. @entity3663 , at least partially, uses @entity2509 pathway to render such effect.

Urotensin upregulates transforming growth factor-b1 expression of XXXX airway through @entity2509 -dependent pathway.

@entity5732 :: ('MESH:C113580', 'Chemical') :: ['U0126'] @entity565 :: ('MESH:D001249', 'Disease') :: ['asthma'] @entity2509 :: ('24338(Tax:10116)', 'Gene') :: ['extracellular signal-regulated kinase', 'ERK'] @entity1810 :: ('59086(Tax:10116)', 'Gene') :: ['TGF-b', 'TGF-b1'] @entity35 :: ('10116', 'Species') :: ['rats'] @entity3663 :: ('29180(Tax:10116)', 'Gene') :: ['UII', 'Urotensin II']
@entity565 :: (MESH:D001249,Disease) :: ['asthma']
