转录组
Wnt信号通路
生物
细胞
串扰
基因
信号转导
下调和上调
细胞生物学
癌症研究
基因表达谱
基因表达
医学
免疫学
遗传学
物理
光学
作者
Rong Tang,Wei Lin,Chanjuan Shen,Xueling Hu,Leilin Yu,Ting Meng,Linlin Zhang,Peter J. Eggenhuizen,Joshua D. Ooi,Peng Jin,Xiang Ding,Xiangcheng Xiao,Yong Zhong
标识
DOI:10.1016/j.intimp.2023.111104
摘要
Hypertensive nephropathy (HTN) is one of the leading causes of end-stage renal disease, yet the molecular mechanisms are still unknown. To explore novel mechanisms and gene targets for HTN, the gene expression profiles of renal biopsy samples obtained from 2 healthy living donor controls and 5 HTN patients were determined by single-cell RNA sequencing. Key hub genes expression were validated by the Nephroseq v5 platform. The HTN endothelium upregulated cellular adhesion genes (ICAM2 and CEACAM1), inflammatory genes (ETS2 and IFI6) and apoptosis related genes (CNN3). Proximal tubules in HTN highly expressed hub genes including BBOX1, TPM1, TMSB10, SDC4, and NUP58, which might be potential novel targets for proximal tubular injury. The upregulated genes in tubules of HTN were mainly participating in inflammatory signatures including IFN-γ signature, NF-κB signaling, IL-12 signaling and Wnt signaling pathway. Receptor-ligand interaction analysis indicated potential cell-cell crosstalk between endothelial cells or mesangial cells with other renal resident cells in HTN. Together, our data identify a distinct cell-specific gene expression profile, pathogenic inflammatory signaling and potential cell-cell communications between endothelial cells or mesangial cells with other renal resident cells in HTN. These findings may provide a promising novel landscape for mechanisms and treatment of human HTN.
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