SLCO2A1 and idiopathic pulmonary fibrosis: Taken together, our results suggest that increased PGE2 in alveolar lumen during BLM-induced lung injury might be efficiently absorbed to ATI cells via SLCO2A1 and that a part of the transported PGE2 is further translocated into interstitial tissue and then reutilized to compensate PGE2 shortage, which could have resulted from defective upregulation of COX-2 as reported in fibroblasts from IPF and rat BLM-induced fibrosis [3].