lithium-chloride and Cicatrix

lithium-chloride has been researched along with Cicatrix* in 1 studies

Other Studies

1 other study(ies) available for lithium-chloride and Cicatrix

Article	Year
Lithium chloride inhibits TGF-β1-induced myofibroblast transdifferentiation via PI3K/Akt pathway in cultured fibroblasts from Tenon's capsule of the human eye. Biotechnology letters, 2014, Volume: 36, Issue:6 Excess scarring of the conjunctiva after glaucoma filtration surgery is a major cause of failure. Transforming growth factor (TGF)-β is critically involved in post-operative scarring. Lithium inhibits TGF-β-induced gene protein expression in corneal fibroblasts and inhibits TGF-β-induced epithelial mesenchymal transition. Here, we investigated the effects of LiCl on TGF-β1-mediated signaling pathways and on myofibroblast transdifferentiation of human Tenon's capsule fibroblasts (HTFs). LiCl treatment reduced expression of TGF-β1-induced α-SMA expression in HTFs. LiCl also decreased Akt phosphorylation induced by TGF-β1. TGF-β1-induced α-SMA expression was significantly decreased by LY294002 and Akt siRNA indicating that these changes are mediated by the PI3K/Akt pathway. Thus, LiCl induces the suppression of transdifferentiation stimulated by TGF-β1 by the regulation of PI3K/Akt signaling in HTFs. Topics: Cell Differentiation; Cicatrix; Fibroblasts; Glaucoma; Humans; Lithium Chloride; Myofibroblasts; Phosphatidylinositol 3-Kinases; Proto-Oncogene Proteins c-akt; Signal Transduction; Tenon Capsule; Transforming Growth Factor beta	2014

Article

Year

Lithium chloride inhibits TGF-β1-induced myofibroblast transdifferentiation via PI3K/Akt pathway in cultured fibroblasts from Tenon's capsule of the human eye.

Biotechnology letters, 2014, Volume: 36, Issue:6

Excess scarring of the conjunctiva after glaucoma filtration surgery is a major cause of failure. Transforming growth factor (TGF)-β is critically involved in post-operative scarring. Lithium inhibits TGF-β-induced gene protein expression in corneal fibroblasts and inhibits TGF-β-induced epithelial mesenchymal transition. Here, we investigated the effects of LiCl on TGF-β1-mediated signaling pathways and on myofibroblast transdifferentiation of human Tenon's capsule fibroblasts (HTFs). LiCl treatment reduced expression of TGF-β1-induced α-SMA expression in HTFs. LiCl also decreased Akt phosphorylation induced by TGF-β1. TGF-β1-induced α-SMA expression was significantly decreased by LY294002 and Akt siRNA indicating that these changes are mediated by the PI3K/Akt pathway. Thus, LiCl induces the suppression of transdifferentiation stimulated by TGF-β1 by the regulation of PI3K/Akt signaling in HTFs.

Topics: Cell Differentiation; Cicatrix; Fibroblasts; Glaucoma; Humans; Lithium Chloride; Myofibroblasts; Phosphatidylinositol 3-Kinases; Proto-Oncogene Proteins c-akt; Signal Transduction; Tenon Capsule; Transforming Growth Factor beta

2014