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: Lefty A protein inhibits TGF-β1-mediated apoptosis in human renal tubular epithelial cells.
    Author: Zheng RP, Bai T, Zhou XG, Xu CG, Wang W, Xu MW, Zhang J.
    Journal: Mol Med Rep; 2013 Aug; 8(2):621-5. PubMed ID: 23807264.
    Abstract:
    This study aimed to examine the effects of Lefty A protein on transforming growth factor-β1 (TGF-β1)-mediated apoptosis in human renal tubular epithelial cells (HK-2). HK-2 cells were transfected with the human Lefty gene to induce the secretion of endogenous Lefty A protein. Following exposure of the HK-2 cells to recombinant human TGF-β1 (10 ng/ml), p-Smad2/3 protein levels were examined by western blot analysis, and cellular apoptosis was detected by flow cytometry 6, 12, 24 and 48 h following TGF-β1 treatment. Coculture of renal tubular epithelial cells with TGF-β1 resulted in a significant increase in p-Smad2/3 protein levels and the rate of cell apoptosis, which were attenuated by liposome-mediated transfection with the Lefty gene. Lefty A protein was able to inhibit the TGF-β1/Smad signaling pathway and markedly attenuate TGF-β1-mediated apoptosis in human renal tubular epithelial cells. Taken together, these results indicated that the TGF-β1/Smad signaling pathway most likely mediates apoptosis in renal tubular epithelial cells. In addition, Lefty A protein is capable of inhibiting the TGF-β1/Smad pathway to reduce TGF-β1/Smad-mediated apoptosis in renal tubular epithelial cells. This study may provide novel insights into the prevention and treatment of urinary tract obstruction disease using Lefty A protein.
    [Abstract] [Full Text] [Related] [New Search]