Cell type and disease specific expression of GPR68 in the human lung

Background: The GPR68 is a transmembrane G-protein coupled receptor sensing protons and thus responding to changes of extracellular acidity. Tissue acidification occurs under hypoxic stress or tissue remodeling, and it is a hallmark in chronic inflammatory lung disease. The role of GPR68 in Asthma and COPD is not well studied. Objective: The role and regulation of the GPR68 in tissues and tissue forming airway cells. Methods: Tissues and primary human lung cells were obtained by endo-bronchial biopsies of 8 controls, 10 asthma and 5 COPD patients. GPR68 expression was determined by three methods: RT-qPCR, immunoblot and immunohistology. Results: GPR68 was expressed by human primary epithelial cells, airway smooth muscle cells (ASMC) and fibroblasts. Cell type specific differences of GPR68 expression were observed by comparing the same diagnosis between different cell types. In control tissues and cells, the GPR68 expression was similar in epithelial and ASMCs, while it was low in fibroblasts. In asthma and COPD derived tissues and cells, the GPR68 expression was highest in epithelial cells, lower in ASMCs and lowest in fibroblasts. Disease specific differences of GPR68 expression were observed by comparing the same cell type between different diagnosis. In epithelial cells, the GPR68 expression was similar in all diagnostic groups, among which COPD patients showed the highest variability. In ASMCs and fibroblasts, the GPR68 expression was highest in control cells and lower in asthmatic and COPD cells. Conclusion: GPR68 expression was cell type and disease specific. This might indicate its contribution to chronic inflammatory lung diseases. It has to be determined if the GPR68 expression correlate with its function.