Fig. 6
From: Divergent roles of prostacyclin and PGE2 in human tendinopathy
Schematic summarizing the key findings. Tendon injury induces a pro-inflammatory state whereby diseased tendon tissues highly express IP receptor, PGIS, COX-2, mPGES-1, NMDAR-1, and PDPN. Tendon stromal cells (CD45negCD34neg) from diseased tendon tissues produce prostacyclin and PGE2 upon treatment with IL-1β, while healthy tendon cells only produce PGE2