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1 Pulmonary and Critical Care Medicine, University of Nebraska Medical Center, Omaha, Nebraska 68198-5125; 2 Pulmonary Division, Internal Medicine, Seoul Adventist Hospital, Seoul 130-650, Korea; and 3 Department of Laboratory and Pulmonary Medicine, Tokyo University, School of Medicine, Tokyo 113-8655, Japan
The controlled accumulation of
fibroblasts to sites of inflammation is crucial to effective tissue
repair after injury. Either inadequate or excessive accumulation of
fibroblasts could result in abnormal tissue function. Prostacyclin
(PGI2) is a potent mediator in the coagulation and
inflammatory processes. The aim of this study was to investigate the
effect of PGI2 on chemotaxis of human fetal lung
fibroblasts (HFL-1). Using the blind well chamber technique, we found
that the PGI2 analog carbaprostacyclin (10
6
M) inhibited HFL-1 chemotaxis to human plasma fibronectin (20 µg/ml)
58.0 ± 13.2% (P < 0.05) and to platelet-derived
growth factor (PDGF)-BB (10 ng/ml) 48.7 ± 4.6% (P < 0.05). Checkerboard analysis demonstrated that carbaprostacyclin
inhibits both directed and undirected migration. The inhibitory effect
of the carbaprostacyclin was concentration dependent and blocked by the
cAMP-dependent protein kinase (PKA) inhibitor KT-5720, suggesting that
a cAMP-PKA pathway may be involved in the process. Two other
PGI2 analogs, ciprostene and dehydro-15-cyclohexyl
carbaprostacyclin (both 106 M), significantly inhibited
fibroblast migration to fibronectin. In summary, PGI2
appears to inhibit fibroblast chemotaxis to fibronectin and PDGF-BB.
Such an effect may contribute to the regulation of fibroblasts in wound
healing and could contribute to the pathogenesis of diseases
characterized by abnormal tissue repair remodeling.
prostaglandin I2; protein kinase; tissue repair; inflammation
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