Microrna-155 Regulates Cockroach Allergen Induced Cyclooxygenase-2 Expression in Airway Epithelium
Sunday, March 6, 2016: 1:30 PM
Room 403B (Convention Center)
Lipeng Qiu, PhD, , , , , , , , ,
Rationale: Exposure to cockroach allergen is a strong risk factor for developing asthma. Reactive oxygen species (ROS) are important mediators in asthma and allergic diseases. Recent studies indicated a link for environmental pollutant/allergen exposure and oxidative stress in epithelium. We sought to investigate whether cockroach allergen can induce oxidative stress in airway epithelium.

Methods: Expression of 84 genes related to oxidative stress was examined in cockroach allergen (CRE)­-treated human primary bronchial epithelial cells (PBECs) by RT2 Profiler PCR array. The differentially expressed genes were further validated in A549 and TC-1, human and mouse lung epithelial cell lines, by qRT-PCR and in lung tissues from cockroach allergen-challenged mouse model of asthma by immunofluoresence staining. The effect of miR-155 on target gene expression and stability was also examined.

Results: Only the COX-2 gene was significantly up-regulated in CRE-treated PBECs among all examined genes. The increased COX-2 was further validated in CRE treated A549 and TC-1. COX-2 was also detected in airway epithelium of CRE-challenged mice by co-staining of COX-2 and EpCAM. Interestingly, microRNA (miR)-155 predicted to target COX-2 showed significantly increased in lung tissues from the same mouse model. miR-155 over-expression in A549 by miR-155 mimic transfection significantly enhanced COX-2 expression at the mRNA and protein levels. An increased COX-2 mRNA stability was found in miR-155 over-expressed TC-1, but not in A549.

Conclusions: These results suggest that COX-2 may be a major gene related to CRE-induced oxidative stress, and that miR-155 may play a role in regulating the COX-2-ROS axis in asthma.