AI Article Synopsis
- The study investigates KyoT2's role in asthma, focusing on airway remodeling and hyperresponsiveness.
- KyoT2, which inhibits Notch signaling, was tested on asthmatic mice to assess its effects on airway structure and resistance.
- Results showed that KyoT2 reduces Hes1 expression, lessens airway remodeling, and improves hyperresponsiveness, suggesting it could be a viable treatment for asthma.
Article Abstract
The typical pathological features of asthma are airway remodeling and airway hyperresponsiveness (AHR). KyoT2, a negative modulator of Notch signaling, has been linked to asthma in several previous studies. However, whether KyoT2 is involved in the regulation of airway remodeling or the modulation of airway resistance in asthma is unclear. In this study, we aimed to evaluate the therapeutic potential of KyoT2 in preventing asthma-associated airway remodeling and AHR. BALB/c mice were used to generate a mouse model of asthma. Additionally, the expression of Hes1 and Notch1 in airway was analyzed using Immunofluorescence examination. The asthmatic mice were intranasally administered adenovirus expressing KyoT2 and were compared to control groups. Furthermore, subepithelial fibrosis and other airway remodeling features were analyzed using hematoxylin and eosin staining, Van Gieson's staining and Masson's trichrome staining. AHR was also evaluated. This study revealed that KyoT2 downregulated the expression of Hes1, repressed airway remodeling, and alleviated AHR in asthmatic mice. It is reasonable to assume that KyoT2 downregulates airway remodeling and resistance in asthmatic mice through a Hes1-dependent mechanism. Therefore, KyoT2 is a potential clinical treatment strategy for asthma.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4713516 | PMC |
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