Fig. 7: CCN2 inhibition by PRS-220 attenuates fibrotic remodeling in a human precision cut lung slice (PCLS) model of IPF. | Nature Communications

Fig. 7: CCN2 inhibition by PRS-220 attenuates fibrotic remodeling in a human precision cut lung slice (PCLS) model of IPF.

From: Preclinical concept studies showing advantage of an inhaled anti-CTGF/CCN2 protein for pulmonary fibrosis treatment

Fig. 7

a Histopathological analysis of CCN2 expression in IPF lung tissue. Representative images of lung tissue sections from n = 16 different IPF patients are shown. b Experimental procedure of PCLS model. Created in BioRender. Pavlidou, M. (2025) https://BioRender.com/b00o965c Experimental design of an ex vivo proof of concept study to investigate the anti-fibrotic effect of CCN2 inhibition by PRS-220 in PCLS from IPF patients. PCLS were treated daily with PRS-220 (100 nM and 500 nM), pamrevlumab (100 nM) and nintedanib (2 µM). Treatment with PRS-220 vehicle served as a control. PCLS were harvested at day 5 for analysis of Collagen1A1 protein levels. Created in BioRender. Pavlidou, M. (2025) https://BioRender.com/y24t356d Collagen1A1 (COL1A1) protein analysis by Western blot with GAPDH serving as a loading control. Figure shows representative immunoblots of experiments performed with lung tissue from n = 3 IPF patients with n = 4-5 technical replicates per IPF donor. Arrows indicate COL1A1 protein bands subjected to densitometric analysis. e Densitometric analysis of COL1A1 signal in Western blots. Single data points show integrated density values (IDV) of COL1A1 signal normalized to loading control GAPDH of all technical replicates from PCLS of in total n = 3 IPF lung tissue donors (n = 4 technical replicates per treatment group for donor 1 & 2 and n = 5 per treatment group for donor 3; Kruskal-Wallis test with Dunn’s multiple comparison; ***p < 0.001, ns (not statistically significant) p > 0.05). Source data are provided as a Source Data file.

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