The Transient Receptor Potential Vanilloid 1 Is Associated with Active Inflammation in Ulcerative Colitis
Autor: | Gabriela Fonseca-Camarillo, Jesús K. Yamamoto-Furusho, Marco A. Villeda-Ramirez, Daniela Meza-Guillen, Joel Toledo-Mauriño, Janette Furuzawa-Carballeda, Rafael Barreto-Zuñiga |
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Jazyk: | angličtina |
Rok vydání: | 2018 |
Předmět: |
Adult
Male 0301 basic medicine Article Subject Colon Immunology TRPV1 TRPV Cation Channels behavioral disciplines and activities Pathogenesis 03 medical and health sciences Transient receptor potential channel 0302 clinical medicine Downregulation and upregulation Gene expression lcsh:Pathology Humans Medicine Gene Inflammation Interleukin-6 business.industry musculoskeletal neural and ocular physiology Cell Biology Middle Aged medicine.disease Immunohistochemistry Ulcerative colitis 030104 developmental biology nervous system Colitis Ulcerative Female 030211 gastroenterology & hepatology lipids (amino acids peptides and proteins) business psychological phenomena and processes lcsh:RB1-214 Research Article |
Zdroj: | Mediators of Inflammation Mediators of Inflammation, Vol 2018 (2018) |
ISSN: | 1466-1861 0962-9351 |
Popis: | The transient receptor potential vanilloid 1 (TRPV1) may play a role in the pathogenesis of ulcerative colitis (UC). The aim of the study was to determine the gene and protein expression of TRPV1 in UC patients and noninflamed controls. Gene expression was performed by RT-PCR, and protein expression was performed by immunohistochemistry. The gene expression of TRPV1 was significantly increased in the remission UC group compared to active UC patients (P=0.002), and an upregulation of the TRPV1 gene was associated with clinical outcomes such as age at diagnosis (P=0.02) and clinical disease course characterized by relapsing and continuous activity (P=0.07). TRPV1 immunoreactive cells were conspicuously higher in all intestinal layers from active UC patients compared with noninflamed control tissue. These findings suggest that TRPV1 might be involved in UC pathogenesis. |
Databáze: | OpenAIRE |
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