Cultured lung fibroblasts isolated from patients with idiopathic pulmonary fibrosis have a diminished capacity to synthesize prostaglandin E2 and to express cyclooxygenase-2.

Abstract

Prostaglandin E2 (PGE2) inhibits fibroblast proliferation and collagen synthesis. In this study, we compared lung fibroblasts isolated from patients with idiopathic pulmonary fibrosis (F-IPF) and from patients undergoing resectional surgery for lung cancer (F-nl) with respect to their capacity for PGE2 synthesis and their expression and regulation of cyclooxygenase (COX)

Prostaglandin E2 Mediates IL-1β-Related Fibroblast Mitogenic Effects in Acute Lung Injury through Differential Utilization of Prostanoid Receptors

“…Lung fibroblast PGE 2 production has been reported previously to be up-regulated at the level of COX-2 in response to mediators of direct relevance to lung injury including LPS, TGF-␤, and IL-1␤ (29,48). However, our data using purified IL-1␤, and inhibitors of IL-1␤ signaling (i.e., IL-1ra and IL-␤-neutralizing Abs) clearly demonstrate that IL-1␤ is the predominant mediator of COX-2 induction and resultant PGE 2 production in adult human lung fibroblasts, in the context of ALI.…”

Is there a role of hypoxemia in penile fibrosis: a viewpoint presented to the Society for the Study of Impotence

“…26 Consistent with this observation, cultured lung ®broblasts from patients suffering from idiopathic pulmonary ®brosis have a diminished capacity to synthesize PGE 2 . 27 In order to establish a cause and effect relationship of PGE in prophylaxis of lung ®brosis, prostaglandin G/H synthase (PGHS, a key enzyme in PGE synthesis) was transfected into rabbits. Animals were treated with pulmonary dosages of bacterial lipopolysaccharide which results in pulmonary hypertension and ®brosis.…”

Success of prostaglandin E 2 in structure–function is a challenge for structure-based therapeutics

“…Distinct from its proinflammatory actions, PGE 2 promotes resolution of inflammation (27). In addition, lung fibroblasts from individuals with pulmonary fibrosis display diminished COX-2 expression and PGE 2 (28). Acute inflammation has four potential outcomes: complete resolution, abscess formation, healing by fibrosis, or progression to chronic inflammation (10).…”