Diminished prostaglandin E2 contributes to the apoptosis paradox in idiopathic pulmonary fibrosis.

ABSTRACT:

Rationale

Patients with idiopathic pulmonary fibrosis (IPF), a progressive disease with a dismal prognosis, exhibit an unexplained disparity of increased alveolar epithelial cell (AEC) apoptosis but reduced fibroblast apoptosis.

Objectives

To examine whether the failure of patients with IPF to up-regulate cyclooxygenase (COX)-2, and thus the antifibrotic mediator prostaglandin (PG)E(2), accounts for this imbalance.

Methods

Fibroblasts and primary type II AECs were isolated from control and fibrotic human lung tissue. The effects of COX-2 inhibition and exogenous PGE(2) on fibroblast and AEC sensitivity to Fas ligand (FasL)-induced apoptosis were assessed.

Measurements and main results

IPF lung fibroblasts are resistant to FasL-induced apoptosis compared with co

SUBMITTER: Maher TM 

PROVIDER: S-EPMC2902759 | biostudies-literature | 2010 Jul

REPOSITORIES: biostudies-literature