ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2010
Transcriptional regulation of CXC-ELR chemokines KC and MIP-2 in mouse pancreatic acini.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.
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Who cites it
27 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.
- Adipose saturation reduces lipotoxic systemic inflammation and explains the obesity paradox.Science advances · 2021Pooled it
- Roles of chemokines in pancreatitis: A review.World journal of gastrointestinal pathophysiology · 2025Review
- Oxidative stress, DAMPs, and immune cells in acute pancreatitis: molecular mechanisms and therapeutic prospects.Frontiers in immunology · 2025Review
- A safe method for rapid therapeutic pancreatic cooling.iScience · 2024Article
- Changes in cytokines and chemokines in an acute pancreatitis model.Ulusal travma ve acil cerrahi dergisi = Turkish journal of trauma & emergency surgery : TJTES · 2024Article
- Experimental animal models of chronic inflammation.Current research in immunology · 2023Review
- Effects of elevated CORespiratory research · 2021Article
- Effect of Docosahexaenoic Acid on CaNutrients · 2019Article
- Small heterodimer partner negatively regulates C-X-C motif chemokine ligand 2 in hepatocytes during liver inflammation.Scientific reports · 2018Article
- c-Src regulates cargo transit via the Golgi in pancreatic acinar cells.Scientific reports · 2018Article
- Inhibition of ubiquitin-activating enzyme protects against organ injury after intestinal ischemia-reperfusion.American journal of physiology. Gastrointestinal and liver physiology · 2018Article
- Chemokine CXCL16 mediates acinar cell necrosis in cerulein induced acute pancreatitis in mice.Scientific reports · 2018Article
- PYR-41, A Ubiquitin-Activating Enzyme E1 Inhibitor, Attenuates Lung Injury in Sepsis.Shock (Augusta, Ga.) · 2018Article
- Macrophage inflammatory protein-2 as mediator of inflammation in acute liver injury.World journal of gastroenterology · 2017Review
- Src kinases play a novel dual role in acute pancreatitis affecting severity but no role in stimulated enzyme secretion.American journal of physiology. Gastrointestinal and liver physiology · 2016Article
- CXCR2 inhibition suppresses acute and chronic pancreatic inflammation.The Journal of pathology · 2015Article
- CXCR1/CXCR2 antagonist CXCL8(3-74)K11R/G31P blocks lung inflammation in swine barn dust-instilled mice.Pulmonary pharmacology & therapeutics · 2015Article
- Role of phosphoinositide 3-kinase in the pathogenesis of acute pancreatitis.World journal of gastroenterology · 2014Review
- Metabolically induced liver inflammation leads to NASH and differs from LPS- or IL-1β-induced chronic inflammation.Laboratory investigation; a journal of technical methods and pathology · 2014Article
- Pancreatitis activates pancreatic apelin-APJ axis in mice.American journal of physiology. Gastrointestinal and liver physiology · 2013Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Neutrophils and their chemoattractants, the CXC-ELR chemokines keratinocyte cytokine (KC) and macrophage inflammatory protein-2 (MIP-2), play a critical role in pancreatitis. While acute pancreatitis is initiated in acinar cells, it is unclear if these are a source of CXC-ELR chemokines. KC and MIP-2 have NF-κB, activator protein-1 (AP-1) sites in their promoter regions. However, previous studies have shown increased basal and reduced caerulein-induced AP-1 activation in harvested pancreatic tissue in vitro, which limits interpreting the caerulein-induced response. Moreover, recent studies suggest that NF-κB silencing in acinar cells alone may not be sufficient to reduce inflammation in acute pancreatitis. Thus the aim of this study was to determine whether acinar cells are a source of KC and MIP-2 and to understand their transcriptional regulation. Primary overnight-cultured murine pancreatic acini were used after confirming their ability to replicate physiological and pathological acinar cell responses. Upstream signaling resulting in KC, MIP-2 upregulation was studied along with activation of the transcription factors NF-κB and AP-1. Cultured acini replicated critical responses to physiological and pathological caerulein concentrations. KC and MIP-2 mRNA levels increased in response to supramaximal but not to physiological caerulein doses. This upregulation was calcium and protein kinase C (PKC), but not cAMP, dependent. NF-κB inhibition completely prevented upregulation of KC but not MIP-2. Complete suppression of MIP-2 upregulation required dual inhibition of NF-κB and AP-1. Acinar cells are a likely source of KC and MIP-2 upregulation during pancreatitis. This upregulation is dependent on calcium and PKC. MIP-2 upregulation requires both NF-κB and AP-1 in these cells. Thus dual inhibition of NF-κB and AP-1 may be a more successful strategy to reduce inflammation in pancreatitis than targeting NF-κB alone.
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Registered trials
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