These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Contrasting roles for BMP-4 and ventromorphins (BMP agonists) in TGFβ-induced lens EMT.
    Author: Shu DY, Ng K, Wishart TFL, Chui J, Lundmark M, Flokis M, Lovicu FJ.
    Journal: Exp Eye Res; 2021 May; 206():108546. PubMed ID: 33773977.
    Abstract:
    Transforming growth factor beta (TGFβ) and bone morphogenetic protein (BMP) signaling play opposing roles in epithelial-mesenchymal transition (EMT) of lens epithelial cells, a cellular process integral to the pathogenesis of fibrotic cataract. We previously showed that BMP-7-induced Smad1/5 signaling blocks TGFβ-induced Smad2/3-signaling and EMT in rat lens epithelial cell explants. To further explore the antagonistic role of BMPs on TGFβ-signaling, we tested the capability of BMP-4 or newly described BMP agonists, ventromorphins, in blocking TGFβ-induced lens EMT. Primary rat lens epithelial explants were treated with exogenous TGFβ2 alone, or in combination with BMP-4 or ventromorphins. Treatment with TGFβ2 induced lens epithelial cells to undergo EMT and transdifferentiate into myofibroblastic cells with upregulated α-SMA and nuclear translocation of Smad2/3 immunofluorescence. BMP-4 was able to suppress this EMT without blocking TGFβ2-nuclear translocation of Smad2/3. In contrast, the BMP agonists, ventromorphins, were unable to block TGFβ2-induced EMT, despite a transient and early ability to significantly reduce TGFβ2-induced nuclear translocation of Smad2/3. This intriguing disparity highlights new complexities in the responsiveness of the lens to differing BMP-related signaling. Further research is required to better understand the antagonistic relationship between TGFβ and BMPs in lens EMT leading to cataract.
    [Abstract] [Full Text] [Related] [New Search]