ArticleScientific reports2025
Deficiency of integrin β4 contributes bronchopulmonary dysplasia by compromising cellular stability through the activation of RhoA-(ZO-1) signaling pathways.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Alterations in the composition and remodeling of the lung extracellular matrix (ECM) are critical for lung development. Our research identified that mice with a conditional knockout of integrin β4 (Itgb4) exhibit lung dysplasia. In this study, we investigated the expression of collagen IV (Col IV) and matrix metalloproteinase 9 (MMP9) in both normal and Itgb4-deficient mice using Western blot and immunohistochemistry techniques. Our findings indicate that Itgb4 deficiency results in bronchopulmonary dysplasia, which is characterized by increased deposition of Col IV and reduced expression of MMP9. The zonula occludens-1 (ZO-1), on both normal and Col IV-coated substrates was assessed using laser confocal microscopy. Concurrently, RhoA activities were quantified via fluorescence resonance energy transfer (FRET) microscopy. The findings indicated a significant disruption of ZO-1 in ITGB4-deficient cells, accompanied by an dcrease in RhoA activity.However, RhoA activity was enhanced in ITGB4
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