SHORT REPORTSIncreased nitric oxide synthesis in ulcerative colitis
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2018, Cell ReportsCitation Excerpt :In addition, NO signaling is important for the host immune response and tissue repair (Brown et al., 1993; Witthöft et al., 1998). Although a substantial increase in NO signaling has been implicated in the pathogenesis of human IBD, the specific cellular origin of NO and the exact roles of epithelial and immune cell-derived NO in intestinal inflammation remain unclear (Boughton-Smith et al., 1993; Kolios et al., 2004; Middleton et al., 1993; Suschek et al., 2004). A primary reason for the limited understanding of the role of cell- and context-dependent NO signaling in IBD is the redundancy of the three isoforms of nitric oxide synthase (NOS): endothelial (eNOS), neuronal (nNOS), and inducible (iNOS).
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2017, Expert Systems with ApplicationsCitation Excerpt :This finding is coherent with the knowledge that iNOS is an important well-known mediator of brain and gut inflammation pathologies. In particular, microscopy analysis gut biopsies from human patients affected by acute gut inflammation, identified higher iNOS expression respect to healthy control subjects (Kolios, Rooney, Murphy, Robertson, & Westwick, 1998; Middleton, Shorthouse, & Hunter, 1993). iNOS was not found in gut non-inflamed samples.