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Pannexin expression in human colon: Alterations in Inflammatory Bowel Disease (IBD)
Abstract   Peer reviewed

Pannexin expression in human colon: Alterations in Inflammatory Bowel Disease (IBD)

E Diezmos, Shaun L Sandow, P P Bertrand and Lu Liu
Neurogastroenterology and Motility, Vol.24(Supplement 2), p.64
International Neurogastroenterology and Motility Meeting, 2012 (Bologna, Italy, 06-Sep-2012–08-Sep-2012)
2012
url
https://doi.org/10.1111/j.1365-2982.2012.01997.xView
Published Version

Abstract

Clinical Sciences Neurosciences pannexin human colon Inflammatory Bowel Disease (IBD)
Objective: Pannexins (PANXs) constitute a new family of gap junction-like proteins. PANXs mainly form hemichannels and participate in cell signalling by release of ATP and ions in response to physiological and pathological stimuli. Three types of PANX proteins, PANX1, 2 and 3, have been identified in human. The aims of the present study were to determine the expression profile of PANXs in the human colon and investigate their potential involvement in the pathophysiology of inflammatory bowel disease. Methods: Real-time PCR and Western blot were performed to determine the expression of PANX genes and proteins in the colonic mucosa and muscle of control, ulcerative colitis (UC) and Crohn's disease (CD). Immunohistochemistry was conducted to localise the cellular distribution of PANX1 and PANX2. Results: Genes for PANX1 and 2 but not for PANX3 were present in both colonic mucosa and muscle with PANX1 being expressed at higher levels than PANX2. PANX1 mRNA was significantly down-regulated in UC muscle, but there were no changes in UC mucosa, CD muscle and mucosa. PANX1 immunoreactivity was present in all layers of the colon, mostly on endocrine glands, epithelial cells, varicose nerve fibres of submucosal and myenteric ganglia, endothelium of blood vessels and erythrocytes. The size and number of PANX1 positive blood vessels were greatly increased in the mucosal and submucosal regions of UC and CD, where a significant PANX1 positive lymphocyte infiltration was also seen. In CD muscle, there was an increase in number and size of PANX1 stained blood vessels and an increase in immunoreactive density of the muscle itself. These observations correlated to the Western blotting results, showing that PANX1 protein was upregulated in CD muscle. PANX2 immunoreactivity was localised to the cell bodies of submucosal and myenteric ganglia, epithelial cells, vascular smooth muscle and leukocytes, but was absent from erythrocytes. PANX2 positive lymphocytic infiltration was greatly increased in UC and CD mucosa and submucosa. Conclusion: These results indicate that PANXs may function as ATP release channels to regulate intestinal blood supply, gut hormone secretion, motility and sensory processing. PANX channels may play a crucial role in the development of intestinal inflammation

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Clinical Neurology
Gastroenterology & Hepatology
Neurosciences

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