Agonist-specific desensitization of PGE₂-stimulated cAMP signaling due to upregulated phosphodiesterase expression in human lung fibroblasts.

ABSTRACT: Pulmonary fibrosis is characterized by fibroblasts persisting in an activated form, producing excessive fibrous material that destroys alveolar structure. The second messenger molecule cyclic 3',5'-adenosine monophosphate (cAMP) has antifibrotic properties, and prostaglandin E₂ (PGE₂) can stimulate cAMP production through prostaglandin E (EP)₂ and EP₄ receptors. Although EP receptors are attractive therapeutic targets, the effects of long-term exposure to PGE₂ have not been characterized. To determine the effects of long-term exposure of lung fibroblasts to PGE₂, human fetal lung (HFL)-1 cells were treated for 24 h with 100 nM PGE₂ or other cAMP-elevating agents. cAMP levels stimulated by acute exposure to PGE

SUBMITTER: Nunez FJ 

PROVIDER: S-EPMC7328663 | biostudies-literature | 2020 May

REPOSITORIES: biostudies-literature