Dipeptidyl peptidase 4 (DPP4) has been proposed as a marker for activated fibroblasts in fibrotic disease. We aimed to investigate whether a profibrotic DPP4 phenotype is present in lung tissue from patients with idiopathic pulmonary fibrosis (IPF). The presence of DPP4 + fibroblasts in normal and IPF lung tissue was investigated using flow cytometry and immunohistology. In addition, the involvement of DPP4 in fibroblast activation was examined in vitro, using CRISPR/Cas9 mediated genetic inactivation to generate primary DPP4 knockout lung fibroblasts. We observed a reduced frequency of primary DPP4 + fibroblasts in IPF tissue using flow cytometry, and an absence of DPP4 + fibroblasts in pathohistological features of IPF. The in vivo observations were supported by results in vitro showing a decreased expression of DPP4 on normal and IPF fibroblasts after profibrotic stimuli (transforming growth factor β) and no effect on the expression of activation markers (α-smooth muscle actin, collagen I and connective tissue growth factor) upon knockout of DPP4 in lung fibroblasts with or without activation with profibrotic stimuli.

Sidor (från-till)1-12
TidskriftFrontiers in Pharmacology
StatusPublished - 2022

Bibliografisk information

Copyright © 2022 Kadefors, Berlin, Wildt, Dellgren, Rolandsson Enes, Aspberg and Westergren-Thorsson.

Ämnesklassifikation (UKÄ)

  • Lungmedicin och allergi


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