Protein steady-state levels of S-adenosylhomocysteine-hydrolase and cystathionine gamma-lyase diminished but methylthioadenosine phosphorylase levels increased in pancreas with acute pancreatitis.
While the pancreas of BTC transgenic mice in the background of Egfr<sup>Wa5/+</sup> is still protected against AP, the BTC-mediated protection is no longer present in the absence of ERBB4.
Soluble urokinase plasminogen activator receptor is of good predictive value for SAP risk and may serve as a potential biomarker for disease severity, inflammation, and inhospital mortality in SAP patients.
Protein steady-state levels of S-adenosylhomocysteine-hydrolase and cystathionine gamma-lyase diminished but methylthioadenosine phosphorylase levels increased in pancreas with acute pancreatitis.
The objectives of this study were to investigate the associations between circulating levels of glucagon, cortisol, and human growth hormone and glucose homeostasis after AP as well as their associations with a comprehensive panel of pancreatic hormones, gut peptides, and proinflammatory cytokines.
The expression patterns of miR-135a and family with sequence similarity 129 member A (FAM129A) in patients with AP were analyzed on the basis of the GEO database.
Our findings reveal, for the first time, that β1 syntrophin is a critical regulator of actin cytoskeleton and autophagy in pancreatic acinar cells and is potently protective against cerulein-induced acute pancreatitis.
Biochemical tests, PON-1 and oxidative stress parameters (malonyl dialdehyde, MDA; superoxide dismutase, SOD; total antioxidant capacity, TAC) were evaluated in the sera of patients with acute pancreatitis at admission (day 0), day 3 and day 10 of follow-up, between June and September 2017.
The onset of AP is characterized by early trypsinogen activation.The present study aimed to investigate the expression of microRNA (miR)‑92a‑3p and early growth response protein 1 (Egr1), and the effect of miR‑92a‑3p on trypsinogen activation in the pancreatic exocrine cell line AR42J. mRNA and miRNA microarrays were used to identify differentially expressed mRNAs and miRNAs in AR42J cells.
Most importantly, we demonstrated that the RIPK1/NF-ĸB/AQP8 axis might be a potential regulatory pathway mediating RIPK1-dependent regulated acinar cell necrosis in early AP.
In this study, we found that the transcriptional activity of p53 was impaired and the expressions of its proapoptotic targets Puma and CD95 were significantly decreased, which explains the apoptosis silencing during AP.
Compared with miR-27a-5p + pcDNA group, transfection of miR-27a-5p mimic and pcDNA-PTEN significantly increased the expression of PTEN (P < 0.05), decreased the apoptotic rate (P < 0.05), and increased the inflammatory response (P < 0.05). miR-27a-5p induced apoptosis and inhibited the inflammatory response of pancreatic acinar cells in AP by targeting PTEN.