CYSLTR1 promotes adenoid hypertrophy by activating ERK1/2
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- Published online on: June 8, 2018 https://doi.org/10.3892/etm.2018.6282
- Pages: 966-970
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Abstract
Cysteinyl leukotriene receptor 1 (CYSLTR1) serves a pivotal role in allergic reactions, which is one of the main causes of adenoid hypertrophy. The present study aimed to investigate the function of CYSLT1 within adenoid hypertrophy. A total of 40 patients with adenoid hypertrophy were recruited between January 2014 and January 2016 at the Children's Hospital of Hebei Province, China. The patients were divided into either the mild‑moderate group or the severe group according to their disease severity. The expression of CYSLT1 in the adenoid tissue and whole blood of all patients and healthy controls was detected by reverse transcription‑quantitative polymerase chain reaction. Associations between the expression level of CYSLT1 and the clinical characteristics of patients were analyzed. Primary human adenoid epithelial cells (HAECs) with CYSLT1 knockdown and overexpression were constructed. The levels of extracellular signal‑regulated kinase (ERK)2 and phosphorylated‑ERK1/2 in adenoid tissue and HAECs were detected by western blot analysis. The expression of CYSLT1 in adenoid tissue and whole blood of all patients with adenoid hypertrophy was significantly higher compared with the healthy controls (P<0.05). In addition, the expression level of CYSLT1 was significantly higher in the severe group compared with the mild‑moderate group (P<0.05). The highest level of p‑ERK1/2 in adenoid tissue was observed in the severe group, followed by the mild‑moderate group and then the control group (P<0.05). CYSLT1 expression was positively associated with the severity of disease. CYSLT1 knockdown significantly decreased the level of p‑ERK1/2 in HAECs (P<0.05), while CYSLT1 overexpression significantly increased the level of p‑ERK1/2. It was concluded that CYSLT1 may contribute to the progression of adenoid hypertrophy by activating ERK1/2.
