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Airway smooth muscle cells from ovalbumin-sensitized mice show increased proliferative response to TGFβ1 due to upregulation of Smad3 and TGFβRII. | LitMetric

AI Article Synopsis

  • This study investigates how Transforming growth factor (TGF)-β1 influences the growth of airway smooth muscle cells (ASMCs) in the context of asthma.
  • Researchers created an allergic model to simulate airway remodeling and analyzed the proliferation of ASMCs using various techniques, including cell counting and western blotting.
  • Findings indicate that ASMCs from asthma-sensitized mice show increased growth in response to TGFβ1, linked to up-regulated proteins Smad3 and TGFβRII, with the process being partly regulated by the ERK1/2 pathway.

Article Abstract

Objective: This study aimed to elucidate the role of Transforming growth factor (TGF)-β1 signaling in the proliferation of airway smooth muscle cells (ASMCs).

Background: TGF-β1 is an important cytokine in airway remodeling in asthma. However, results of studies focusing on the effect of TGFβ1 on proliferation of ASMCs are controversial.

Methods: An allergic model that mimics airway remodeling in chronic asthma was established and primary ASMCs were cultured. Cell proliferation was detected by viable cell counting and Cell Counting Kit (CCK)-8 analysis. Expression and phosphorylation of Smad3, type 1 TGFβ receptor (TGFβRI), type 2 TGFβ receptor (TGFβRII), extracellular signal-regulated kinase (ERK)-1/2, p38 mitogen-activated protein kinase (MAPK), C-Jun N-terminal kinase (JNK) and AKT were detected by western blot. siRNAs were used to knock down Smad3 and TGFβRII.

Results: Smad3 and TGFβRII were up-regulated in primary ASMCs isolated from ovalbumin (OVA)-sensitized mice as compared with ASMCs isolated from unsensitized control mice, which persisted for at least four passages. TGFβ1 stimulated proliferation of ASMCs isolated from OVA-sensitized mice, which was inhibited by specific siRNA targeting Smad3 or TGFβRII. However ASMCs from control mice showed no proliferative response to TGFβ1. TGFβ1-induced proliferation of ASMCs from OVA-sensitized mice was markedly attenuated by PD-98059, a specific ERK1/2 inhibitor. TGFβ1 induced ERK1/2 phosphorylation within 15 minute, which was partially blocked by specific inhibitor of Smad3 (SIS3).

Conclusions: ASMCs isolated from OVA-sensitized mice showed hyper-proliferation upon TGFβ1 stimulation. This might have been associated with up-regulated Smad3 and TGFβRII and mediated by ERK1/2 downstream to Smad3.

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Source
http://dx.doi.org/10.1080/02770903.2016.1225760DOI Listing

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