The Korean journal of internal medicine

  • 제32권6호
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  • Pages.1053-1061
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  • 2017
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  • 1226-3303(pISSN)
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  • 2005-6648(eISSN)
대한내과학회 (The Korean Association of Internal Medicine)
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DOI QR코드

DOI QR Code

Blocking junctional adhesion molecule C promotes the recovery of cisplatin-induced acute kidney injury

  • Kim, Sun Chul (Division of Nephrology, Department of Internal Medicine, Korea University Anam Hospital) ;
  • Ko, Yoon Sook (Division of Nephrology, Department of Internal Medicine, Korea University Anam Hospital) ;
  • Lee, Hee Young (Division of Nephrology, Department of Internal Medicine, Korea University Anam Hospital) ;
  • Kim, Myung-Gyu (Division of Nephrology, Department of Internal Medicine, Korea University Anam Hospital) ;
  • Jo, Sang-Kyung (Division of Nephrology, Department of Internal Medicine, Korea University Anam Hospital) ;
  • Cho, Won-Yong (Division of Nephrology, Department of Internal Medicine, Korea University Anam Hospital)
  • 투고 : 2016.02.25
  • 심사 : 2016.04.25
  • 발행 : 2017.11.01
⟨ 이전 논문 다음 논문 ⟩

초록

Background/Aims: Recent findings have demonstrated the occurrence of neutrophil transendothelial migration in the reverse direction (reverse TEM) and that endothelial junctional adhesion molecule C (JAM-C) is a negative regulator of reverse TEM. In this study, we tested the effects of a JAM-C blocking antibody on the resolution of kidney injuries and inflammation in a mouse model of cisplatin-induced acute kidney injury (AKI). Methods: Cisplatin was administered via intraperitoneal injection. A JAM-C blocking antibody or a control immunoglobulin G was administered intraperitoneal at 1.5 mg/kg, with the injection being delayed until day 4 following cisplatin administration to restrict the effect of antibodies on recovery. Results: After cisplatin injection, serum creatinine and histologic injuries peaked on day 4. Treatment with a JAM-C blocking antibody on days 4 and 5 promoted the functional and histologic recovery of cisplatin-induced AKI on days 5 and 6. Facilitating recovery with a JAM-C blocking antibody correlated with significantly increased circulating intercellular adhesion molecule $_1{^+}$ Tamm-Horsfall $protein^+$ neutrophils and significantly decreased renal neutrophil infiltration, indicating that facilitating reverse the TEM of neutrophils from the kidney to the peripheral circulation partially mediated the resolution of inflammation and recovery. Conclusions: These results demonstrated that reverse TEM is involved in the resolution of neutrophilic inflammation in cisplatin-induced AKI and that JAM-C is an important regulator of this process.

키워드

참고문헌

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피인용 문헌

  1. Recent Advances in Models, Mechanisms, Biomarkers, and Interventions in Cisplatin-Induced Acute Kidney Injury vol.20, pp.12, 2017, https://doi.org/10.3390/ijms20123011
  2. Caveolin-2 in urine as a novel biomarker of renal recovery after cisplatin induced nephrotoxicity in rats vol.313, pp.None, 2019, https://doi.org/10.1016/j.toxlet.2019.07.010