Severe ischemia-reperfusion injury induces epigenetic inactivation of LHX1 in kidney progenitor cells after kidney transplantation.

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Tác giả: Ana Amaya-Garrido, María Berdasco, Núria Bolaños, Sergi Codina, Carlos Couceiro, Josep M Cruzado, Núria Doladé, Montserrat Gomà, James S Heald, Anna Manonelles, Angelika Merkel, Miguel L Pato, David Piñeyro, Carlos Quero-Dotor, Paola Romagnani, Fernando E Setién, Anna Sola, Cristian Varela, Francesc Vigués

Ngôn ngữ: eng

Ký hiệu phân loại: 636.0885 Animal husbandry

Thông tin xuất bản: United States : American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons , 2025

Mô tả vật lý:

Bộ sưu tập: NCBI

ID: 215843

Severe ischemia-reperfusion injury (IRI) causes acute and chronic kidney allograft damage. As therapeutic interventions to reduce damage are limited yet, research on how to promote kidney repair has gained significant interest. To address this question, we performed genome-wide transcriptome and epigenome profiling in progenitor cells isolated from the urine of deceased (severe IRI) and living (mild IRI) donor human kidney transplants and identified LIM homeobox-1 (LHX1) as an epigenetically regulated gene whose expression depends on the IRI severity. Using a mouse model of IRI, we observed a relationship between IRI severity, LHX1 promoter hypermethylation, and LHX1 gene expression. Using functional studies, we confirmed that LHX1 expression is involved in the proliferation of epithelial tubular cells and podocyte differentiation from kidney progenitor cells. Our results provide evidence that severe IRI may reduce intrinsic mechanisms of kidney repair through epigenetic signaling.
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