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Inhibition of HDAC3 protects against kidney cold storage/transplantation injury and allograft dysfunction.
Xiang, Xiaohong; Dong, Guie; Zhu, Jiefu; Zhang, Gang; Dong, Zheng.
Afiliación
  • Xiang X; Department of Nephrology, Hunan Key Laboratory of Kidney Disease and Blood Purification, The Second Xiangya Hospital at Central South University, Changsha, China.
  • Dong G; Department of Cellular Biology and Anatomy, Medical College of Georgia at Augusta University and Charlie Norwood VA Medical Center, Augusta, GA, U.S.A.
  • Zhu J; Department of Cellular Biology and Anatomy, Medical College of Georgia at Augusta University and Charlie Norwood VA Medical Center, Augusta, GA, U.S.A.
  • Zhang G; Department of Nephrology, Hunan Key Laboratory of Kidney Disease and Blood Purification, The Second Xiangya Hospital at Central South University, Changsha, China.
  • Dong Z; Center of Nephrology and Dialysis, Transplantation, Renmin Hospital of Wuhan University, Wuhan, China.
Clin Sci (Lond) ; 136(1): 45-60, 2022 01 14.
Article en En | MEDLINE | ID: mdl-34918039
Cold storage/rewarming is an inevitable process for kidney transplantation from deceased donors, which correlates closely with renal ischemia-reperfusion injury (IRI) and the occurrence of delayed graft function. Histone deacetylases (HDAC) are important epigenetic regulators, but their involvement in cold storage/rewarming injury in kidney transplantation is unclear. In the present study, we showed a dynamic change of HDAC3 in a mouse model of kidney cold storage followed by transplantation. We then demonstrated that the selective HDAC3 inhibitor RGFP966 could reduce acute tubular injury and cell death after prolonged cold storage with transplantation. RGFP966 also improved renal function, kidney repair and tubular integrity when the transplanted kidney became the sole life-supporting graft in the recipient mouse. In vitro, cold storage of proximal tubular cells followed by rewarming induced remarkable cell death, which was suppressed by RGFP966 or knockdown of HDAC3 with shRNA. Inhibition of HDAC3 decreased the mitochondrial pathway of apoptosis and preserved mitochondrial membrane potential. Collectively, HDAC3 plays a pathogenic role in cold storage/rewarming injury in kidney transplantation, and its inhibition may be a therapeutic option.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Fenilendiaminas / Acrilamidas / Daño por Reperfusión / Trasplante de Riñón / Histona Desacetilasas Límite: Animals Idioma: En Revista: Clin Sci (Lond) Año: 2022 Tipo del documento: Article País de afiliación: China Pais de publicación: Reino Unido
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Fenilendiaminas / Acrilamidas / Daño por Reperfusión / Trasplante de Riñón / Histona Desacetilasas Límite: Animals Idioma: En Revista: Clin Sci (Lond) Año: 2022 Tipo del documento: Article País de afiliación: China Pais de publicación: Reino Unido