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Cell profiling of mouse acute kidney injury reveals conserved cellular responses to injury

Kirita, Yuhei ; Wu, Haojia ; Uchimura, Kohei ; Wilson, Parker C. ; Humphreys, Benjamin D.

Proceedings of the National Academy of Sciences - PNAS, 2020-07, Vol.117 (27), p.15874-15883 [Periódico revisado por pares]

United States: National Academy of Sciences

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Título:
Cell profiling of mouse acute kidney injury reveals conserved cellular responses to injury
Autor: Kirita, Yuhei ; Wu, Haojia ; Uchimura, Kohei ; Wilson, Parker C. ; Humphreys, Benjamin D.
Assuntos: Acute Kidney Injury - genetics ; Acute Kidney Injury - metabolism ; Acute Kidney Injury - pathology ; Aging ; Allografts ; Animal models ; Animals ; Biological Sciences ; Cell signaling ; Communication networks ; Disease Models, Animal ; Fibrosis ; Gene Regulatory Networks ; Gene sequencing ; Humans ; Inflammation ; Injuries ; Kidney - injuries ; Kidney - metabolism ; Kidney diseases ; Kidney transplantation ; Kidney Tubules, Proximal - injuries ; Kidney Tubules, Proximal - metabolism ; Kidney Tubules, Proximal - pathology ; Kidneys ; Male ; Mice ; Mice, Inbred C57BL ; Nuclei (cytology) ; Rats ; Repair ; Ribonucleic acid ; RNA ; Sequence Analysis, RNA ; Stroma ; Stromal Cells - metabolism ; Stromal Cells - pathology ; Therapeutic applications ; Transcription ; Transcriptome
É parte de: Proceedings of the National Academy of Sciences - PNAS, 2020-07, Vol.117 (27), p.15874-15883
Notas: ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
Author contributions: Y.K. and B.D.H. designed research; Y.K., H.W., and K.U. performed research; Y.K. contributed new reagents/analytic tools; Y.K., H.W., K.U., P.C.W., and B.D.H. analyzed data; and B.D.H. wrote the paper.
Edited by Martin R. Pollak, Beth Israel Deaconess Medical Center, Brookline, MA, and approved May 20, 2020 (received for review March 25, 2020)
Descrição: After acute kidney injury (AKI), patients either recover or alternatively develop fibrosis and chronic kidney disease. Interactions between injured epithelia, stroma, and inflammatory cells determine whether kidneys repair or undergo fibrosis, but the molecular events that drive these processes are poorly understood. Here, we use single nucleus RNA sequencing of a mouse model of AKI to characterize cell states during repair from acute injury. We identify a distinct proinflammatory and profibrotic proximal tubule cell state that fails to repair. Deconvolution of bulk RNA-seq datasets indicates that this failed-repair proximal tubule cell (FR-PTC) state can be detected in other models of kidney injury, increasing during aging in rat kidney and over time in human kidney allografts. We also describe dynamic intercellular communication networks and discern transcriptional pathways driving successful vs. failed repair. Our study provides a detailed description of cellular responses after injury and suggests that the FR-PTC state may represent a therapeutic target to improve repair.
Editor: United States: National Academy of Sciences
Idioma: Inglês

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Cell profiling of mouse acute kidney injury reveals conserved cellular responses to injury

Kirita, Yuhei ; Wu, Haojia ; Uchimura, Kohei ; Wilson, Parker C. ; Humphreys, Benjamin D.

United States: National Academy of Sciences

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