Single-cell transcriptomics reveals activation of endothelial cell and identifies LHPP as a potential target in ulcerative colitis
Ruoyu He,
Yanfei Wang,
Chen Shuang,
Chan Xu,
Xiaoling Li,
Yanfei Cao
Affiliations
Ruoyu He
Department of Gastroenterology, The Third Affiliated Hospital of Zhejiang Chinese Medical University, No. 219 Moganshan Road, Xihu District, Hangzhou Zhejiang, 310005, Zhejiang Province, China
Yanfei Wang
Department of Gastroenterology, The Third Affiliated Hospital of Zhejiang Chinese Medical University, No. 219 Moganshan Road, Xihu District, Hangzhou Zhejiang, 310005, Zhejiang Province, China
Chen Shuang
Department of Neurology, The Third Affiliated Hospital of Zhejiang Chinese Medical University, No. 219 Moganshan Road, Xihu District, Hangzhou, 310005, Zhejiang Province, China
Chan Xu
Clinical Laboratory, The Third Affiliated Hospital of Zhejiang Chinese Medical University, No. 219 Moganshan Road, Xihu District, Hangzhou, 310005, Zhejiang Province, China
Xiaoling Li
Elder Medicine Department, The Third Affiliated Hospital of Zhejiang Chinese Medical University, No. 219 Moganshan Road, Xihu District, Hangzhou, 310005, Zhejiang Province, China
Yanfei Cao
Department of Gastroenterology, The Third Affiliated Hospital of Zhejiang Chinese Medical University, No. 219 Moganshan Road, Xihu District, Hangzhou Zhejiang, 310005, Zhejiang Province, China; Corresponding author.
This study delves into Ulcerative colitis (UC), a persistent gastrointestinal disorder marked by inflammation and ulcers, significantly elevating colorectal cancer risk. The emergence of single-cell RNA sequencing (scRNA-seq) technology has opened new avenues for dissecting the intricate cellular dynamics and molecular mechanisms at play in UC pathology. By analyzing scRNA-seq data from individuals with UC, our study has revealed a consistent enhancement of inflammatory response pathways throughout the course of the disease, alongside detailing the characteristics of endothelial cell damage within colitis environments. A noteworthy finding is the downregulation of Phospholysine Phosphohistidine Inorganic Pyrophosphate Phosphatase (LHPP), which exhibited a inversely correlate with STAT3 expression levels. The markedly reduced expression of LHPP in both the tissues and plasma of UC patients positions LHPP as a compelling target for therapeutic intervention. Our findings highlight the pivotal role LHPP could play in moderating inflammation, spotlighting its potential as a crucial molecular target in the quest to understand and treat UC.
