ArticleCell communication and signaling : CCS2014
Pancreatic T cell protein-tyrosine phosphatase deficiency ameliorates cerulein-induced acute pancreatitis.
Article in Cell communication and signaling : CCS, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- Inhibition of PTP1B Through NADH Dehydrogenase Activity Reduces Acute Pancreatic Acinar Cell Pyroptosis by Inhibiting the ROS/TXNIP/NLRP3 Pathway.Digestive diseases and sciences · 2026Article
- STATs Signaling Pathways in Acute Pancreatitis: Mechanisms and Regulation.International journal of medical sciences · 2026Review
- COVID-19 cytokine storm: The anger of inflammation.Cytokine · 2020Review
- The role of T-cell protein tyrosine phosphatase in epithelial carcinogenesis.Molecular carcinogenesis · 2019Review
- Intracellular IL-37b interacts with Smad3 to suppress multiple signaling pathways and the metastatic phenotype of tumor cells.Oncogene · 2017Article
- Pancreatic Protein Tyrosine Phosphatase 1B Deficiency Exacerbates Acute Pancreatitis in Mice.The American journal of pathology · 2016Article
- Idiopathic pancreatitis in a patient with a STAT3 mutation.Allergy & rhinology (Providence, R.I.) · 2016Article
- Pancreatic T cell protein-tyrosine phosphatase deficiency affects beta cell function in mice.Diabetologia · 2015Article
- The conspiracy of autophagy, stress and inflammation in acute pancreatitis.Current opinion in gastroenterology · 2014Review
- Article
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Authors and funding
11 authors at 3 institutions in 3 countries.
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Abstract
backgroundAcute pancreatitis (AP) is a common clinical problem whose incidence has been progressively increasing in recent years. Onset of the disease is trigged by intra-acinar cell activation of digestive enzyme zymogens that induce autodigestion, release of pro-inflammatory cytokines and acinar cell injury. T-cell protein tyrosine phosphatase (TCPTP) is implicated in inflammatory signaling but its significance in AP remains unclear.
resultsIn this study we assessed the role of pancreatic TCPTP in cerulein-induced AP. TCPTP expression was increased at the protein and messenger RNA levels in the early phase of AP in mice and rats. To directly determine whether TCPTP may have a causal role in AP we generated mice with pancreatic TCPTP deletion (panc-TCPTP KO) by crossing TCPTP floxed mice with Pdx1-Cre transgenic mice. Amylase and lipase levels were lower in cerulein-treated panc-TCPTP KO mice compared with controls. In addition, pancreatic mRNA and serum concentrations of the inflammatory cytokines TNFα and IL-6 were lower in panc-TCPTP KO mice. At the molecular level, panc-TCPTP KO mice exhibited enhanced cerulein-induced STAT3 Tyr705 phosphorylation accompanied by a decreased cerulein-induced NF-κB inflammatory response, and decreased ER stress and cell death.
conclusionThese findings revealed a novel role for pancreatic TCPTP in the progression of cerulein-induced AP.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.