Slco2a1, also known as PGT, OATP2A1, PHOAR2, or SLC21A2, is a plasma membrane transporter with 12 transmembrane domains. It ubiquitously expressed in tissues, mediates the membrane transport of prostaglandins (PGs, mainly PGE2, PGF2α, PGD2) and thromboxanes (e.g., TxB2), and is involved in the metabolic clearance of prostaglandins. PGs imported by it are oxidized by cytoplasmic 15-hydroxyprostaglandin dehydrogenase. SLCO2A1 is also part of the Maxi-Cl channel, regulating anion fluxes [1,5].

SLCO2A1-related knockout studies are not directly mentioned in the provided abstracts. However, whole-exome analyses suggest that recessive inheritance of its mutations is associated with primary hypertrophic osteoarthropathy (PHO) and chronic enteropathy associated with SLCO2A1 (CEAS). In PHO, mutations in SLCO2A1 disturb PGE2 catabolism, leading to increased circulating PGE2 levels. In CEAS, multiple ulcers in the small intestine with chronic bleeding and protein loss occur, likely due to elevated PGE2 levels [1,2,3,4].

In conclusion, Slco2a1 is crucial for the transport and metabolism of prostaglandins. Its mutations are associated with PHO and CEAS, highlighting its significance in these disease conditions. Understanding Slco2a1 can potentially provide new insights into the pathophysiology of these refractory diseases and guide the development of targeted therapies [1,2,3,4].