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Binding of leukotriene C/sub 4/ to rat lung fibroblasts and stimulation of collagen synthesis in vitro

Journal Article · · Biochemistry; (United States)
OSTI ID:7142873

Although prostaglandins of the E series, which are products of the cyclooxygenase pathway, have been known as inhibitors or down-regulators of fibroblasts proliferation and collagen synthesis, the more recently discovered products of the 5-lipoxygenase pathway have not been as extensively investigated with regard to fibroblast function. In this study, a sulfidopeptide product of the lipoxygenase pathway, leukotriene C/sub 4/ (LTC/sub 4/), was examined for its ability to modulate rat lung fibroblasts collagen synthesis and proliferation in vitro. The data revealed the ability of LTC/sub 4/ and to a lesser extent leukotriene D/sub 4/ (LTD/sub 4/) to stimulate collagen synthesis in a dose-dependent manner with affecting cellular proliferation as determined by radiolabeled thymidine incorporation; 1 nM LTC/sub 4/ caused an 85% increase above untreated controls in (/sup 3/H)proline incorporation into collagenous protein in the media, which was blocked by the putative leukotriene receptor antagonist FPL55712 (10 ..mu..M) and inhibited by cycloheximide and actinomycin D. Binding of (/sup 3/H(LTC/sub 4/ to these cells was specific, reversible, and saturable. Under equilibrium conditions, there was an estimated 2.39 x 10/sup 4/ receptors per cell. This binding was also inhibited by 10 ..mu..M FPL55712. Competitive binding studies show specificity of this binding for LTC/sub 4/ relative to LTD/sub 4/ and FPL55712. Furthermore, no significant conversion of LTC/sub 4/ to LTD/sub 4/ or leukotriene E/sub 4/ was noted during the binding studies. These results indicate the presence of specific LTC/sub 4/ receptors on these cells which may mediate the cellular effects on protein and collagen synthesis.

Research Organization:
Univ. of Michigan, Ann Arbor (USA)
OSTI ID:
7142873
Journal Information:
Biochemistry; (United States), Journal Name: Biochemistry; (United States) Vol. 27:8; ISSN BICHA
Country of Publication:
United States
Language:
English