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: Knockdown of lncRNA SNHG1 attenuated Aβ25-35-inudced neuronal injury via regulating KREMEN1 by acting as a ceRNA of miR-137 in neuronal cells.
    Author: Wang H, Lu B, Chen J.
    Journal: Biochem Biophys Res Commun; 2019 Oct 20; 518(3):438-444. PubMed ID: 31447119.
    Abstract:
    Alzheimer's disease (AD) is a chronic neurodegenerative disease featured by progressive memory loss and cognitive dysfunction. Long non-coding RNAs are recently demonstrated as important regulatory molecules in neurodegenerative diseases. This study explored regulatory role of lncRNA small nucleolar RNA host gene 1 (SNHG1) in the neuronal cell injury induced by Aβ25-35. Our results showed that Aβ25-35 inhibited cell viability, induced cell apoptosis and increased the expression of SNHG1 in SH-SY5Y and human primary neuron (HPN) cells. Knockdown of SNHG1 partially reversed the effects of Aβ25-35 treatment on cell viability, cell apoptosis, mitochondrial membrane potential (MMP), caspase-3 activity, and apoptosis signaling-related protein levels in SH-SY5Y and HPN cells. The bioinformatics analysis and luciferase reporter assay showed that SNHG1 functioned as competing endogenous RNA (ceRNA) for miR-137, and pre-treatment with SNHG1 siRNA increased cell viability, suppressed cell apoptosis, increased MMP, decreased caspase-3 activity and caused a decrease in the protein levels of cytochrome C and cleaved caspase-3 and an increase in Bcl-2 protein level in the Aβ25-35-treated SH-SY5Y and HPN cells, which was significantly attenuated by the presence of miR-137 mimics. Moreover, miR-137 negatively regulated the expression of kringle containing transmembrane protein 1 (KREMEN1) via targeting its 3' untranslated region, and knockdown of SNHG1 also suppressed KREMEN1 in SH-SY5Y and HPN cells. Overexpression of KREMEN1 impaired the neuronal protective effects of SNHG1 knockdown in the Aβ25-35-treated SH-SY5Y and HPN cells. In summary, our result indicated that knockdown of SNHG1 exerted its neuronal protective effects via repressing KRENEN1 by acting as a ceRNA for miR-137 in the in vitro cell model of AD.
    [Abstract] [Full Text] [Related] [New Search]