Pancreatic stellate cell (PSC) activation is a major cause of chronic pancreatitis and pancreatic cancer, yet the mechanisms by which PSCs switch from quiescent to activated state are poorly studied. In this study, we identified JUN, a key transcription factor that maintains the quiescent state of PSCs, by integrating single-cell sequencing data from multiple pancreatic tissues and using WGCNA and SCENIC algorithms, and demonstrated that the expression and activity of JUN is a major regulator of the quiescent state of PSCs through cellular experiments and multiple pancreatic-related disease bulk RNAseq data. This study explores the main mechanism of PSC activation and provides a theoretical basis for the treatment of multiple pancreatic injury-related diseases caused by PSCs.
View Article and Find Full Text PDFBackground: Circulating endothelial progenitor cells (EPCs) play important roles in vascular repair. However, the mechanisms of high-glucose- (HG-) induced cord blood EPC senescence and the role of B2 receptor (B2R) remain unknown.
Methods: Cord blood samples from 26 patients with gestational diabetes mellitus (GDM) and samples from 26 healthy controls were collected.
Objective: To observe the effect of acupuncture therapy on 14-3-3, Bcl-2 and Bax expression levels in the cerebral cortex in neonatal rats with hypoxic-ischemic brain damage(HIBD).
Methods: Timed pregnant Sprague-Dawley rat dams were delivered either vaginally (normal group), or by C-section (sham-operation group) or by C-section with 5 min of global anoxia (anoxia group), with 8 rats in each group. The rat pups of the anoxia group were randomly divided into model group and acupuncture group (n =8).