open access articleChronic obstructive pulmonary disease (COPD) constitutes a major cause of morbidity and
mortality. Genome wide association studies have shown significant associations between airflow
obstruction or COPD with a non-synonymous SNP in the TNS1 gene, which encodes tensin1.
However, the expression, cellular distribution and function of tensin1 in human airway tissue and
cells are unknown. We therefore examined these characteristics in tissue and cells from controls
and people with COPD or asthma.
Airway tissue was immunostained for tensin1. Tensin1 expression in cultured human
airway smooth muscle cells (HASMCs) was evaluated using qRT-PCR, western blotting and
immunofluorescent staining. siRNAs were used to downregulate tensin1 expression.
Tensin1 expression was increased in the airway smooth muscle and lamina propria in COPD
tissue, but not asthma, when compared to controls. Tensin1 was expressed in HASMCs and
upregulated by TGFβ1. TGFβ1 and fibronectin increased the localisation of tensin1 to fibrillar
adhesions. Tensin1 and α-smooth muscle actin (αSMA) were strongly co-localised, and tensin1
depletion in HASMCs attenuated both αSMA expression and contraction of collagen gels.
In summary, tensin1 expression is increased in COPD airways, and may promote airway
obstruction by enhancing the expression of contractile proteins and their localisation to stress
fibres in HASMCs
