Publications by authors named "Kalyani Kasisomayajula"
Article Synopsis
- The Smad2/3 pathway is crucial for how TGF-beta1 prevents branching morphogenesis and promotes CTGF expression in developing lungs.
- Researchers studied how inhibiting the JNK pathway affects TGF-beta1's ability to activate Smad2 and influence lung development in mouse embryos.
- Results showed that JNK inhibition enhances Smad2 activity, decreases normal branching, promotes CTGF expression, and causes cell death, suggesting that the JNK pathway may counteract the effects of TGF-beta1 on lung development.
High tidal volume (V(T)) ventilation plays a key role in ventilator induced lung injury and bronchopulmonary dysplasia. However, little is known about the effect of high V(T) on expression of growth factors that are critical to lung development. In a previous study, we demonstrated that connective tissue growth factor (CTGF) inhibits branching morphogenesis.
View Article and Find Full Text PDFArticle Synopsis
- Transforming growth factor-beta1 (TGF-beta1) is identified as a key negative regulator of lung branching morphogenesis, influencing growth processes in developing lungs.
- Researchers found that TGF-beta1 not only inhibits branching morphogenesis but also induces the expression of connective tissue growth factor (CTGF), which mediates this inhibitory effect.
- The study also revealed that inhibiting the TGF-beta signaling pathway with SB431542 could reverse the effects of TGF-beta1 and promote normal lung branching, highlighting the role of the TbetaRI/ALK-5-dependent Smad2 signaling pathway in this process.