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Abstract: SA-PO177

Coronin 1α Remodels Inflammatory Microenvironment to Dictate AKI Prognosis

Session Information

  • AKI: Mechanisms - III
    November 04, 2023 | Location: Exhibit Hall, Pennsylvania Convention Center
    Abstract Time: 10:00 AM - 12:00 PM

Category: Acute Kidney Injury

  • 103 AKI: Mechanisms


  • Gui, Yuan, University of Connecticut School of Medicine, Farmington, Connecticut, United States
  • Wang, Yuanyuan, University of Connecticut School of Medicine, Farmington, Connecticut, United States
  • Wang, Jack L., University of Connecticut School of Medicine, Farmington, Connecticut, United States
  • Zhou, Dong, University of Connecticut School of Medicine, Farmington, Connecticut, United States

T-cell-mediated immune response is a key mechanism in AKI onset. Our proteomics data indicate that coronin-1α is markedly induced in the kidneys after AKI, and it is highly expressed in T cells and macrophages to regulate immune cell activation, migration, and phagocytosis. As a protein first noted for its role in modulating actin dynamics and pathogen-host interactions, coronin-1α is spread throughout the cytoplasm and the cell cortex when the cell is resting. Once a pathogen enters the cell, coronin-1α binds to the phagosomal membrane, ensuring the binding and activation of calcineurin, ultimately stopping the fusion of lysosomes with phagosomes. Whether coronin-1α plays a role in AKI is unknown.


Male and female coronin-1α knockout (Coro1A-/-) mice were used to induce AKI by renal ischemia-reperfusion injury (IRI) at 1, 2, and 3 days (d) or cisplatin at 3d, respectively. A 3-month IRI model was constructed to evaluate AKI long-term outcomes in Coro1A-/- mice. AKI patients samples were employed. Global-/phospho-proteomics and single-nucleus RNA-Seq were utilized.


After AKI, serum creatinine and blood urea nitrogen levels were largely preserved in Coro1A-/- mice compared with wild-type mice. Kidney morphological damages and the expression of the tubular injury markers and chemocytokines were consistently decreased in Coro1A-/- mice. Knockout coronin 1α effectively increased the clearance of apoptotic cells by macrophages. As a consequence, tubular cell proliferation was enhanced in Coro1A-/- mice. In the 3-month IRI model, Coro1A-/- mice exhibited significantly improved kidney function, histology and less fibrotic lesions. Mechanistically, global and phospho-proteomics revealed that inflammation-related signaling pathways were repressed after deleting coronin 1α, and T-lymphokine-activated killer-cell-originated protein kinase (TOPK) was the topmost differentially expressed protein in Coro1A-/- mice diseased kidneys. Single-nucleus RNA-Seq showed higher expression of TOPK in the isolated Coro1A-/- immune cells. In vivo and ex vivo, TOPK regulated an inflammatory microenvironment formation, enhancing apoptotic neutrophil clearance and providing favorable conditions to prime tubule repair and regeneration.


Coronin 1α is vital in determining AKI prognosis, and TOPK is a potential immune checkpoint in mitigating AKI.


  • NIDDK Support