Prostaglandin (PG)E2 exhibits antifibrotic activity in vocal fold fibroblasts.
Prostaglandin (PG)E2 exhibits antifibrotic activity in vocal fold fibroblasts.
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前列腺素 (PG)E2 在声带成纤维细胞中表现出抗纤维化活性。
DOI:
10.1002/lary.21795
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发表时间:
2011
期刊:
影响因子:
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通讯作者:
Branski,RyanC
中科院分区:
文献类型:
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作者:
Zhou,Hang;Felsen,Diane;Sandulache,VladC;Amin,MilanR;Kraus,DennisH;Branski,RyanC
Objectives/HypothesisProstaglandin (PG)E2has been implicated in a variety of disease processes. It has been described as antifibrotic in the lower airway, yet scar‐inducing in the skin. We seek to describe the effects of PGE2on vocal fold fibroblasts and its interactions with transforming growth factor (TGF)‐β1. In addition, we describe a novel organotypic model, a critical step in the development of therapeutic trials.Study DesignIn vitro, ex vivo.MethodsCollagen secretion by human vocal fold fibroblasts (HVFF) was assayed in response to TGF‐β1, PGE2, and specific EP receptor agonists. Basal HVFF migratory rate was also quantified in response to PGE2. TGF‐β1 induced COX‐2 mRNA expression/PGE2secretion was assayed. Excised vocal folds were subjected to exogenous IL‐1β; PGE2secretion into the supernatant was then assayed.ResultsTGF‐β1‐induced collagen secretion was blunted in a dose‐dependent manner in response to PGE2. This effect appears to be mediated primarily through the EP1 and EP2 receptors. TGF‐β1 induced COX‐2 mRNA expression and PGE2secretion. In our organ culture model, IL‐1β stimulated PGE2secretion in a dose‐dependent manner.ConclusionsPGE2is antifibrotic; this finding suggests that the upper airway response to this inflammatory mediator differs significantly from the lower airway. These data have important clinical implications for a variety of pathological processes. Furthermore, exogenous TGF‐β1 elicits induction of COX‐2, suggesting inherent complexity regarding these processes and PGE2signaling, specifically. In addition, our organ culture model may prove useful as a means to quantify biological phenomena in the vocal folds.