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. 2018 May 25;9:2066. doi: 10.1038/s41467-018-04336-z

Fig. 4.

Fig. 4

Modeling the biomechanics of traction bronchiectasis. a Schematic shows the formation of numerous cystic airspaces in the fibrotic lung interstitium due to traction force-induced bronchial dilation. b The bronchial dilation was modeled through inducing the dilation of tissue openings in engineered fibrotic microtissues. FE simulated first principal stress distribution of a square microtissue supported by flexible micropillars (c), a square microtissue supported by rigid micropillars (d) and a long microtissue supported by rigid micropillars (e). Note high stress concentration around the micropillars in d and e induced dilation of the tissue opening. f Overview of the strategy for fibrosis induction in long microtissue and fibrosis evaluation based on the measurement of stress concentration and tissue opening size. g Merged immunofluorescence images of α-SMA and collagen type-I of untreated and TGF-β1-treated long microtissues. Apparent dilation of openings around micropillars and in the belly region can be observed in TGF-β1-treated condition. Scale bar is 500 µm. h Enlarged views of collagen type-I and α-SMA of highlighted region in g. α-SMA positive myofibroblasts aligned circumferentially around the dilated openings, matched well with the direction of simulated principal stress vectors (i). j Plot of the percentage of microtissue area occupied by the openings. The opening area of TGF-β1-treated sample is significantly larger than that of untreated sample at day 6. Data are reported as the mean ± SD. n ≥ 5; *P < 0.001 when compared to untreated condition by one-way ANOVA with Tukey test