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Title: DPPC regulates COX-2 expression in monocytes via phosphorylation of CREB

Journal Article · · Biochemical and Biophysical Research Communications
 [1];  [2]; ; ;  [1];  [2];  [3]
  1. Cardiff School of Health Sciences, University of Wales Institute Cardiff, Western Avenue, Llandaff, Cardiff, Wales CF5 2YB (United Kingdom)
  2. School of Medicine, Cardiff University, Cardiff CF14 4XN (United Kingdom)
  3. Centre for Research in Biomedicine, UWE, Bristol BS16 1QY (United Kingdom)

The major phospholipid in pulmonary surfactant dipalmitoyl phosphatidylcholine (DPPC) has been shown to modulate inflammatory responses. Using human monocytes, this study demonstrates that DPPC significantly increased PGE{sub 2} (P < 0.05) production by 2.5-fold when compared to untreated monocyte controls. Mechanistically, this effect was concomitant with an increase in COX-2 expression which was abrogated in the presence of a COX-2 inhibitor. The regulation of COX-2 expression was independent of NF-{kappa}B activity. Further, DPPC increased the phosphorylation of the cyclic AMP response element binding protein (CREB; an important nuclear transcription factor important in regulating COX-2 expression). In addition, we also show that changing the fatty acid groups of PC (e.g. using L-{alpha}-phosphatidylcholine {beta}-arachidonoyl-{gamma}-palmitoyl (PAPC)) has a profound effect on the regulation of COX-2 expression and CREB activation. This study provides new evidence for the anti-inflammatory activity of DPPC and that this activity is at least in part mediated via CREB activation of COX-2.

OSTI ID:
21143698
Journal Information:
Biochemical and Biophysical Research Communications, Vol. 370, Issue 1; Other Information: DOI: 10.1016/j.bbrc.2008.03.052; PII: S0006-291X(08)00524-X; Copyright (c) 2008 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
Country of Publication:
United States
Language:
English