Shock (Augusta, Ga.) · 2026
Opsonic Peptide MOP3 Attenuates Ischemic Acute Kidney Injury.
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Tenet Megan, Jin Hui, Aziz Monowar, Wang Ping
Аннотация
BACKGROUND: Renal ischemia/reperfusion (I/R) induced acute kidney injury (AKI) is a common and serious condition characterized by renal dysfunction, inflammation, tubular injury, and cell death. Extracellular cold-inducible RNA-binding protein (eCIRP) is a damage-associated molecular pattern that contributes to inflammation and tissue injury. MFG-E8-derived oligopeptide 3 (MOP3) is an opsonic peptide that binds eCIRP and promotes its phagocytic clearance. Here, we investigated the therapeutic effects of MOP3 in a murine model of renal I/R-induced AKI.
METHODS: Mice were subjected to 30 minutes of bilateral renal ischemia and treated with MOP3 or vehicle at the onset of reperfusion. Blood and kidney tissues were collected 20 h later. Renal inflammation, kidney function, tubular injury markers, histological damage, and cell death were assessed by RT-qPCR, biochemical assays, Western blotting, hematoxylin and eosin staining, and TUNEL staining.
RESULTS: MOP3 treatment reduced circulating eCIRP by 40% and renal IL-6, IL-1β, MIP-2, and KC mRNA expression by 43%, 84%, 73%, and 69%, respectively, compared with vehicle treatment. Serum urea nitrogen, creatinine, and NGAL levels were reduced by 56%, 63%, and 44%, respectively, after MOP3 treatment. MOP3 also decreased renal KIM-1 and NGAL mRNA expression by 88% and 44% and reduced their protein levels by 29% and 45%, respectively. Furthermore, MOP3 attenuated renal tubular injury and decreased TUNEL-positive cells.
CONCLUSIONS: These findings demonstrate that MOP3 attenuates inflammation, renal dysfunction, tubular injury, and cell death following renal I/R, suggesting that MOP3 may represent a promising therapeutic strategy for ischemic AKI.
METHODS: Mice were subjected to 30 minutes of bilateral renal ischemia and treated with MOP3 or vehicle at the onset of reperfusion. Blood and kidney tissues were collected 20 h later. Renal inflammation, kidney function, tubular injury markers, histological damage, and cell death were assessed by RT-qPCR, biochemical assays, Western blotting, hematoxylin and eosin staining, and TUNEL staining.
RESULTS: MOP3 treatment reduced circulating eCIRP by 40% and renal IL-6, IL-1β, MIP-2, and KC mRNA expression by 43%, 84%, 73%, and 69%, respectively, compared with vehicle treatment. Serum urea nitrogen, creatinine, and NGAL levels were reduced by 56%, 63%, and 44%, respectively, after MOP3 treatment. MOP3 also decreased renal KIM-1 and NGAL mRNA expression by 88% and 44% and reduced their protein levels by 29% and 45%, respectively. Furthermore, MOP3 attenuated renal tubular injury and decreased TUNEL-positive cells.
CONCLUSIONS: These findings demonstrate that MOP3 attenuates inflammation, renal dysfunction, tubular injury, and cell death following renal I/R, suggesting that MOP3 may represent a promising therapeutic strategy for ischemic AKI.