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ORIGINAL RESEARCH ARTICLE

Polyenoic Fatty Acid Ratios Alter Fibroblast Collagen Production Via PGE₂ and PGE Receptor Subtype Response

Department of Basic Medical Sciences, Purdue University, West Lafayette, Indiana 47907

To whom requests for reprints should be addressed at ¹ Purdue University, Department of Basic Medical Sciences, 625 Harrison Street, West Lafayette, IN 47907-2026. E-mail: turekj{at}purdue.edu

Previous experiments have shown that dietary n-6 and n-3 polyenoic fatty acids (PFA) have different effects on collagen production, a process that may be related to the formation of prostaglandins (PG). This study tested the hypothesis that fibroblast collagen production could be regulated by different n- 6:n-3 PFA ratios and that the effects were mediated by PGE₂ and altered signaling via the different PGE receptor subtypes. Compared to a bovine serum albumin control, eicosapentaenoic acid (EPA; 20:5 n-3) treated cells significantly (P < 0.05) increased both collagen production and collagen as a percentage of total cellular protein (C-PTP), but arachidonic acid (AA; 20:4 n-6) reduced collagen production and C-PTP. As the amount of AA decreased and that of EPA increased, collagen production and C-PTP increased, especially when ratio of n-6:n-3 PFA was less than 1:1. C-PTP was significantly correlated with the amount of PGE₂ in the medium. AA- or EPA-treated cells produced similar C-PTP when incubated with 10^–6 M indomethacin, a cyclooxygenase inhibitor. Addition of exogenous PGE₂ to cell cultures treated with 10^–6 M indomethacin for 48 hrs decreased C-PTP in both AA and EPA groups. Decreased C-PTP was observed in AA-treated cells exposed to EP1, EP2, and EP4 PGE receptor agonists and in EPA-treated cells exposed to EP2 and EP4 agonists. AA-treated cell responded to activators of cyclic adenosine monophosphate and protein kinase C by decreasing C-PTP, but EPA-treated cells were unresponsive. In conclusion, collagen production in 3T3-Swiss fibroblasts induced by different n-6:n-3 PFA ratios was correlated with PGE₂ production and altered responsiveness and signaling via the different PGE receptor subtypes.

Key Words: collagen • PGE₂ • omega-3 fatty acids • omega-6 fatty acids • fibroblast

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