ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2013
Transient receptor potential ankyrin 1 mediates chronic pancreatitis pain in mice.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 51 citations in OpenAlex.
- AAT-MSC-EVs: Novel implications for suppressing ferroptosis, fibrosis and pain associated with chronic pancreatitis.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Uncovering the therapeutic potential of anti-tuberculoid agent Isoniazid in a model of microbial-driven Crohn's disease.Journal of Crohn's & colitis · 2025Article
- Pancreatitis pain quality changes at year 1 follow-up, but GP130 remains a biomarker for pain.Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.] · 2024Article
- The Role of TRP Channels in Sepsis and Colitis.International journal of molecular sciences · 2024Review
- Recent advances in the understanding and management of chronic pancreatitis pain.Journal of pancreatology · 2024Review
- Peripheral Neuroinflammation and Pain: How Acute Pain Becomes Chronic.Current neuropharmacology · 2024Review
- Molecular mechanisms of pain in acute pancreatitis: recent basic research advances and therapeutic implications.Frontiers in molecular neuroscience · 2023Review
- Review
- Nobel somatosensations and pain.Pflugers Archiv : European journal of physiology · 2022Review
- Anterior Cingulate Cortex Mediates Hyperalgesia and Anxiety Induced by Chronic Pancreatitis in Rats.Neuroscience bulletin · 2022Article
- Serum biomarkers for chronic pancreatitis pain patterns.Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.] · 2021Article
- A Novel Cellular Therapy to Treat Pancreatic Pain in Experimental Chronic Pancreatitis Using Human Alpha-1 Antitrypsin Overexpressing Mesenchymal Stromal Cells.Biomedicines · 2021Article
- Selective inhibition of soluble TNF using XPro1595 relieves pain and attenuates cerulein-induced pathology in mice.BMC gastroenterology · 2021Article
- A Mouse Model for Chronic Pancreatitis via Bile Duct TNBS Infusion.Journal of visualized experiments : JoVE · 2021Article
- TRPA1 as a therapeutic target for nociceptive pain.Expert opinion on therapeutic targets · 2020Review
- Transient receptor potential ankyrin 1 contributes to somatic pain hypersensitivity in experimental colitis.Scientific reports · 2020Article
- Nucleus tractus solitarius mediates hyperalgesia induced by chronic pancreatitis in rats.World journal of gastroenterology · 2019Article
- Animal Models: Challenges and Opportunities to Determine Optimal Experimental Models of Pancreatitis and Pancreatic Cancer.Pancreas · 2019Review
- Pros and Cons of Clinically Relevant Methods to Assess Pain in Rodents.Neuroscience and biobehavioral reviews · 2019Review
- TRPA1 Antagonists for Pain Relief.Pharmaceuticals (Basel, Switzerland) · 2018Review
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
Chronic pancreatitis (CP) is a devastating disease characterized by persistent and uncontrolled abdominal pain. Our lack of understanding is partially due to the lack of experimental models that mimic the human disease and also to the lack of validated behavioral measures of visceral pain. The ligand-gated cation channel transient receptor potential ankyrin 1 (TRPA1) mediates inflammation and pain in early experimental pancreatitis. It is unknown if TRPA1 causes fibrosis and sustained pancreatic pain. We induced CP by injecting the chemical agent trinitrobenzene sulfonic acid (TNBS), which causes severe acute pancreatitis, into the pancreatic duct of C57BL/6 trpa1(+/+) and trpa1(-/-) mice. Chronic inflammatory changes and pain behaviors were assessed after 2-3 wk. TNBS injection caused marked pancreatic fibrosis with increased collagen-staining intensity, atrophy, fatty replacement, monocyte infiltration, and pancreatic stellate cell activation, and these changes were reflected by increased histological damage scores. TNBS-injected animals showed mechanical hypersensitivity during von Frey filament probing of the abdomen, decreased daily voluntary wheel-running activity, and increased immobility scores during open-field testing. Pancreatic TNBS also reduced the threshold to hindpaw withdrawal to von Frey filament probing, suggesting central sensitization. Inflammatory changes and pain indexes were significantly reduced in trpa1(-/-) mice. In conclusion, we have characterized in mice a model of CP that resembles the human condition, with marked histological changes and behavioral measures of pain. We have demonstrated, using novel and objective pain measurements, that TRPA1 mediates inflammation and visceral hypersensitivity in CP and could be a therapeutic target for the treatment of sustained inflammatory abdominal pain.
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