E-Prostanoid Receptor Distribution in Airway Smooth Muscle Cells of a Rat Model of Asthma

Airway remodeling is a main pathological characteristic of asthma, and strongly associated with migration and proliferation of airway smooth muscle cells. E-prostanoid (EP) receptor can regulate airway remodeling. This study established a rat model of asthma and evaluated EP changes in airway smooth muscle cells under the asthmatic state so as to provide theoretical evidence for developing EP drugs to treat airway remodeling in asthma. A total of 20 clean Sprague-Dawley rats were randomly assigned to asthma group and control group. 28 days later, they were sacrificed for histological examination. Airway smooth muscle cells were isolated, cultured and measured using quantitative fluorescent PCR. Histopathological examination revealed that rat models of asthma were in accordance with the manifestations of asthmatic airway remodeling. After reverse transcription, real-time quantitative fluorescent PCR was performed using miRNA Q-PCR diagnostic kit. GAPDH was considered the internal reference. Relative expressions of E-prostanoid 1–4 (EP1–4) (2-△△Ct) in the control and asthma groups were respectively as follows: EP1: 4.35±0.18, 6.55±1.21; EP2: 3.64±0.12, 1.35±1.06; EP3: 4.59±1.14, 5.89±1.74; EP4: 2.89±1.85, 1.69±0.44. EP2/4 significantly decreased, but EP1 significantly increased in the asthma group (P < 0.01). These results suggested that the reduced EP2/4 and increased EP1 expressions in airway smooth muscle cells of rat models of asthma were probably important factors for asthmatic airway remodeling.