Single-cell transcriptomics of the mouse kidney reveals potential cellular targets of kidney disease

single cell sequencing;SNS;单细胞测序;单细胞多组学

浏览次数：23 分享：

Jihwan Park, Rojesh Shrestha, Chengxiang Qiu, Ayano Kondo, Shizheng Huang, Max Werth, Mingyao Li, Jonathan Barasch, Katalin Suszták

期刊 Science
时间 2018
影响因子 63.714
起止号 360(6390):758-763.
种属 Mouse
技术平台单细胞测序
样本类型 Vascular endothelial cell
研究方向技术分享
细胞类型内皮细胞
检测基因 TCIM, NA, ACER2, ACVL1, ADA15, ATS5, AGRL2, AGRL4, AMOL1, APBB2, AQP1, ARGL1, RHG31, ARHGF, ARI5B, AT133, NA, BMPR2, NA, CALRL, NA, CSKI2, CC85B, OX2G, NA, CLM9, CD34, CD38, C1QR1, BORG1, CADH5, CDN1A, CLD15, CLC14, CLC1A, CLC2D, CLIC4, CKLF8, COFA1, CO4A1, CO4A2, EFC4A, CRIP2, CTL2A, X3CL1, NA, CP20A, CYYR1, DDAH2, DDT4L, DKK2, RHG07, DLL4, DOCK6, DRAM1, DUS3, ECE1, ECSCR, EDNRB, EFNA1, EFNB2, EGFL7, EHD3, ELK3, MUCEN, EGLN, ENHO, EPAS1, EPHB4, ESAM, EVA1B, NA, PAR1, FA8, FABP4, NA, F110A, F117B, F167B, INKA1, TNR6, FGD5, FKB1A, VGFR1, GLT18, GFRP, GIMA5, GIMA6, CXA4, GBG11, HDBP1, GRASP, NA, GSTM1, HECW2, HEG1, HSPB1, PGBM, HYAL2, ICAM2, ID1, ID3, IFI44, IBP5, IMDH1, ITA6, NA, JAM3, PLAK, KANK3, NA, VGFR2, KLF7, LDB2, LEG9, LIFR, LIMC1, LIMS2, RBTN2, LRC8A, LRC8C, LTBP1, LY6C1, MRP, MEIS2, NA, MGLL, MMRN2, MAD4, MYCT1, MYO1C, NOSTN, NOTC1, NPDC1, NRP1, OAZ2, PBX1, NA, PDE2A, PDGFB, PECA1, PI16, TPA, PLCB1, PLK2, PLPP1, PLPP3, PLS1, PLS2, PLS4, RPC7L, PREX2, NA, PTPRB, PTPRG, RAMP2, RAMP3, RPGF4, NA, NA, RAIN, RBMS1, RADI, RHOB, RHOC, RHOJ, RSAD2, S10AG, S1PR1, SASH1, NA, NA, SEM6A, SERPH, SGK1, 3BP5, SHE, S43A3, SC6A6, SO2A1, SLFN5, SMAD6, SYUG, SNRK, SOX17, SOX18, SPRL1, SPTB2, STMN2, ST1A1, NA, TBX3, ITF2, TIE2, TGFR2, TRBM, TIE1, TIMP3, TINAL, LFG3, TMEM2, TM204, TMM26, TMM88, BACD2, TRI47, TSN7, UN45B, USBP1, VDAC3, XIAP, ZEB1
数据库ID UBERON_0002113

Abstract

Our understanding of kidney disease pathogenesis is limited by an incomplete molecular characterization of the cell types responsible for the organ's multiple homeostatic functions. To help fill this knowledge gap, we characterized 57,979 cells from healthy mouse kidneys by using unbiased single-cell RNA sequencing. On the basis of gene expression patterns, we infer that inherited kidney diseases that arise from distinct genetic mutations but share the same phenotypic manifestation originate from the same differentiated cell type. We also found that the collecting duct in kidneys of adult mice generates a spectrum of cell types through a newly identified transitional cell. Computational cell trajectory analysis and in vivo lineage tracing revealed that intercalated cells and principal cells undergo transitions mediated by the Notch signaling pathway. In mouse and human kidney disease, these transitions were shifted toward a principal cell fate and were associated with metabolic acidosis.

金课堂之文献解析文献原文请点击

技术文章更多

研究领域更多

热点文献

首页 >

技术资源 >

文献中心 >

Abstract