KIM-1-mediated anti-inflammatory activity is preserved by MUC1 induction in the proximal tubule during ischemia-reperfusion injury
Mohammad M. Al‐bataineh, Carol L. Kinlough, Zaichuan Mi, Edwin K. Jackson, Stephanie M. Mutchler, David R. Emlet, John A. Kellum, Rebecca P. Hughey
Abstract
KIM-1 plays a key role in the recovery of the tubule epithelium during renal IRI by mediating efferocytosis and associated signaling that suppresses inflammation. Excessive cleavage of KIM-1 by ADAM17 provides a decoy receptor that aggravates efferocytosis and subsequent signaling. Our data from experiments in mice, patients, and cultured cells show that MUC1 is also induced during IRI and competes with KIM-1 for cleavage by ADAM17. Consequently, MUC1 protects KIM-1 anti-inflammatory activity in the damaged kidney.
Topics & Concepts
IschemiaReperfusion injuryMedicineInternal medicineCardiologyNanoparticle-Based Drug DeliveryAdenosine and Purinergic SignalingSignaling Pathways in Disease