FTX Inhibited PIEZO1 Expression to Alleviate the Senescence and Promote the Growth of Neural Progenitor Cells

Abstract

Background: Intervertebral disc degeneration (IDD) is the leading cause of low back pain. Nucleus pulposus cells (NPCs) play a key role in the production and maintenance of intervertebral disc stroma. This work probed into the role of long non-coding RNAs (lncRNAs) five prime to Xist (FTX) in NPCs and explored its effect on IDD. Methods: The intracellular localization of FTX was determined by fluorescence in situ hybridization (FISH) assay. NPCs were transfected with FTX overexpression plasmid, small interfering FTX (siFTX) and small interfering piezo-type mechanosensitive ion channel component 1 (siPIEZO1). FTX, PIEZO and transient receptor potential vanilloid 4 (TRPV4) expressions were detected through Western blot and quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Cell viability, apoptosis and senescence were assessed by cell counting kit-8 (CCK-8), flow cytometry and β-galactosidase (β-gal) staining assays. Results: FTX was downregulated in IDD and localized in the nucleus of NPCs. FTX knockdown decreased cell viability and increased apoptosis rate, the proportion of β-gal positive cells and PIEZO1 expression in NPCs (p < 0.05), whereas FTX overexpression showed the opposite consequences (p < 0.05). Contrary to the functions of FTX knockdown, silencing PIEZO1 elevated cell viability whereas reduced apoptosis rate, the proportion of β-gal positive cells and TRPV4 level in NPCs (p < 0.05), which also reversed the effects of FTX knockdown on those aspects above (p < 0.05). Conclusions: FTX mitigates apoptosis and senescence in NPCs by suppressing PIEZO1 expression to alleviate IDD in vitro.