Highlighting fibroblast plasticity in lung fibrosis: the WI-38 cell line as a model for investigating the myofibroblast and lipofibroblast switch

Background: Myofibroblasts (MYFs) are generally considered the principal culprits in excessive extracellular matrix deposition and scar formation in the pathogenesis of lung fibrosis. Lipofibroblasts (LIFs), on the other hand, are defined by their lipid-storing capacity and are predominantly found in the alveolar regions of the lung. They have been proposed to play a protective role in lung fibrosis. We previously reported that a LIF to MYF reversible differentiation switch occurred during fibrosis formation and resolution. In this study, we tested whether WI-38 cells, a human embryonic lung fibroblast cell line, could be used to study fibroblast differentiation towards the LIF or MYF phenotype and whether this could be relevant for idiopathic pulmonary fibrosis (IPF). Methods: Using WI-38 cells, Fibroblast (FIB) to MYF differentiation was triggered using TGF-

• Vásquez-Pacheco, E.
• Marega, M.
• Lingampally, A.
• Fassy, J.
• Truchi, M.
• Goth, K.
• Trygub, L.
• Taghizadeh, S.
• Bartkuhn, M.
• Alexopoulos, I.
• Dong, Y.
• Lebrigand, K.
• Gunther, A.
• Chen, C.
• Zhang, J.
• Chao, C. M.
• Al Alam, D.
• El Agha, E.
• Mari, B.
• Bellusci, S.
• Rivetti, S.