Pdcd4 modulates markers of macrophage alternative activation and airway remodeling in antigen-induced pulmonary inflammation

• DOI: 10.1189/jlb.3a0313-136rrr
• Publication Date: 2014-08-06T03:16:58Z
• Authors: Bo Zhong; Xudong Yang; Qingzhu Sun; Li Liu; Xi Lan; Jia Tian; Qirui He; Wei Hou; Haiyan Liu; Congshan Jiang; Ning Gao; Shemin Lu
• Keywords: 0301 basic medicine; Arginase; Ovalbumin; Macrophage Activation; Asthma; Cell Line; Rats; 3. Good health; Disease Models, Animal; Mucus; 03 medical and health sciences; Gene Expression Regulation; Macrophages, Alveolar; Nerve Growth Factor; Airway Remodeling; Animals; RNA Interference; RNA, Small Interfering; Apoptosis Regulatory Proteins; Bronchoalveolar Lavage Fluid; Lung; Biomarkers; Spleen

Abstract Pdcd4 has been known as a tumor-suppressor gene initially and is up-regulated during apoptosis. Surprisingly, we found that was differentially expressed in the lung from E3 rats with AIPI, an animal model for asthma, but precise role of AIPI still remained to be defined. In present study, first evaluated expression control RT-qPCR, Western blot, immunohistochemistry. Then, investigated effects intervention on markers macrophage alternative activation airway remodeling. Upon challenging OVA, tissue AIPI. Immunohistochemistry results showed alveolar macrophages epithelia protein. Overexpression rat cell line, NR8383 cells, increased mRNA arginase-1 TGF-β1, which are activation. response RNAi Fizz1, Ym1/2, arginase-1, TGF-β1 decreased significantly. addition, led decrease BALF cells. Finally, knockdown suppressed eosinophil infiltration, bronchus collagen deposition, mucus production. Overall, these suggest may worthy further investigation target remodeling allergic pulmonary inflammation.