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Articles in PresS, published online ahead of print November 13, 2001
Am J Physiol Cell Physiol, 10.1152/ajpcell.00388.2001
Submitted on August 10, 2001
Accepted on November 8, 2001
1 Internal Medicine, University of Texas Medical Branch, Galveston, Texas, USA
2 Pathology, University of Texas Medical Branch, Galveston, Texas, USA
3 Internal Medicine, University of Texas Medical Branch, Galveston, Texas, USA; Physiology and Biophysics, University of Texas Medical Branch, Galveston, Texas, USA
* To whom correspondence should be addressed. E-mail: rmifflin{at}utmb.edu.
Elevated mucosal IL-1 levels are frequently seen during acute and chronic intestinal inflammation and IL-1 neutralization lessens the severity of inflammation. One major effect of IL-1 is the increased release of eicosanoid mediators via induction of cyclooxygenase-2 (COX-2). One site of COX-2 derived prostaglandin synthesis during acute and chronic intestinal inflammation is the intestinal myofibroblast. COX-2 expression has also been documented in these cells in colonic neoplasms. Thus an understanding of the regulation of COX-2 expression in human intestinal myofibroblasts is important. As an initial step towards this goal we have characterized IL-1
signaling pathways that induce COX-2 expression in cultured human intestinal myofibroblasts. IL-1 treatment resulted in a dramatic transcriptional induction of COX-2 gene expression. Activation of NF-
B, Erk, and p38 signaling pathways was necessary for optimal COX-2 induction. In contrast to what occurs in other cell types, including other myofibroblasts such as renal mesangial cells, PKC inhibition did not prevent IL-1 induced NF-B, or MAPK/SAPK activation, suggesting a novel role for PKC isoforms during this process. The stimulatory effects of PKC, NF-B, Erk-1/2, and presumably JNK activation were exerted at the transcriptional level, while p38 activation resulted in increased stability of the COX-2 message. We conclude that in intestinal myofibroblasts, IL-1-mediated induction of COX-2 expression is a complex process which requires input from multiple signaling pathways. Each parallel pathway acts in relative autonomy, the sum of their actions culminating in a dramatic increase in COX-2 transcription and message stability.
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