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: Circ-UQCRC2 aggravates lipopolysaccharide-induced injury in human bronchial epithelioid cells via targeting miR-495-3p/MYD88-mediated inflammatory response and oxidative stress.
    Author: Zhang X, Chen C, Li B, Lu W.
    Journal: Autoimmunity; 2021 Dec; 54(8):483-492. PubMed ID: 34499003.
    Abstract:
    Infantile pneumonia is a common inflammatory disease with the infections of various pathogens in lower respiratory tracts. Here, the role and working mechanism of circular RNA (circRNA) ubiquinol-cytochrome c reductase core protein 2 (circ-UQCRC2; hsa_circ_0038467) in infantile pneumonia were investigated. Cell viability, apoptosis, and inflammatory response were assessed by 3-(4,5-dimethyl-thiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, flow cytometry, and enzyme-linked immunosorbent assay (ELISA). Cell oxidative stress was analyzed by measuring the production of malondialdehyde (MDA) and superoxide dismutase (SOD). Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and Western blot assay were performed to determine the expression of RNAs and proteins. Dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay were performed to confirm the interaction between microRNA-495-3p (miR-495-3p) and circ-UQCRC2 or myeloid differentiation primary response protein 88 (MYD88). Lipopolysaccharide (LPS) treatment suppressed the viability while induced the apoptosis, inflammation, and oxidative stress of 16HBE cells in a dose-dependent manner. LPS exposure dose-dependently up-regulated the expression of circ-UQCRC2 in 16HBE cells. Circ-UQCRC2 absence attenuated LPS-induced injury in 16HBE cells. miR-495-3p was a target of circ-UQCRC2, and circ-UQCRC2 silencing-mediated protective effects in LPS-induced 16HBE cells were partly reversed by anti-miR-495-3p. MYD88 was a target of miR-495-3p, and MYD88 overexpression partly counteracted miR-495-3p accumulation-mediated influences in 16HBE cells upon LPS exposure. Circ-UQCRC2 interference decreased the protein expression of MYD88 partly by up-regulating miR-495-3p in LPS-induced 16HBE cells. In conclusion, circ-UQCRC2 contributed to LPS-induced injury of 16HBE cells by targeting miR-495-3p/MYD88 signalling-mediated inflammatory response and oxidative stress.
    [Abstract] [Full Text] [Related] [New Search]