Matches in SemOpenAlex for { <https://semopenalex.org/work/W2757029003> ?p ?o ?g. }
- W2757029003 endingPage "7360" @default.
- W2757029003 startingPage "7355" @default.
- W2757029003 abstract "Our previous study found that glucosylceramide, a type of sphingolipids, was associated with liver inflammation and fibrosis. Glucosylceramide is generated by glucosylceramide synthase (GCS), which is encoded by the UDP‑glucose ceramide glucosyltransferase (UGCG) gene. GCS is a key enzyme to regulate the physiological activity of cells. However, the role of GCS in hepatic cells remains unclear. The aim of the present study was to explore the mechanism of GCS in the proliferation and apoptosis of liver cells. Following the interference of expression of GCS in vitro by UGCG small interfering (si)RNA, the MTT method was performed to detect the proliferation of HL‑7702 hepatocytes, and ELISA was used to determine the concentration of tumor necrosis factor (TNF) α and cytochrome c in the supernatant of culture system. Fluorescence microscopy was used to observe the apoptosis of liver cells stained by Annexin V‑fluorescein isothiocyanate/propidium iodide. Reverse transcription‑quantitative polymerase chain reaction was used to detect the gene expression apoptosis regulator Bcl‑2 (Bcl‑2), apoptosis regulator Bax (Bax) and caspase-3. Western blot analysis was used to detect the expression of caspase-3 protein in the liver cells. Following treatment with UGCG siRNA for 24 h, the proliferation of HL‑7702 hepatocytes was significantly inhibited when compared with the transfection reagent group. Furthermore, the early and advanced apoptosis of liver cells showed an increasing trend. Additionally, concentrations of TNF α and cytochrome c showed no significant difference between the UGCG siRNA and transfection reagent groups. Compared with the transfection reagent group, Bcl‑2 mRNA expression decreased, and Bax and caspase-3 mRNA expression increased in the UGCG siRNA transfection group. The protein expression level of caspase-3 showed increased in hepatocytes following the treatment with UGCG siRNA. In conclusion, the metabolic changes of sphingolipids caused by the lack of GCS may be involved in the proliferation and apoptosis of liver cells through the Bcl‑2/Bax signaling pathway." @default.
- W2757029003 created "2017-10-06" @default.
- W2757029003 creator A5000979147 @default.
- W2757029003 creator A5004641991 @default.
- W2757029003 creator A5023492006 @default.
- W2757029003 creator A5032229723 @default.
- W2757029003 creator A5043185825 @default.
- W2757029003 creator A5052676364 @default.
- W2757029003 creator A5060337298 @default.
- W2757029003 creator A5077471484 @default.
- W2757029003 creator A5082789515 @default.
- W2757029003 date "2017-05-01" @default.
- W2757029003 modified "2023-10-14" @default.
- W2757029003 title "Glucosylceramide synthase regulates the proliferation and apoptosis of liver cells in vitro by Bcl-2/Bax pathway" @default.
- W2757029003 cites W173798027 @default.
- W2757029003 cites W1965094655 @default.
- W2757029003 cites W1966452335 @default.
- W2757029003 cites W1966758841 @default.
- W2757029003 cites W1969158591 @default.
- W2757029003 cites W1976417809 @default.
- W2757029003 cites W1976777085 @default.
- W2757029003 cites W2000043946 @default.
- W2757029003 cites W2008757142 @default.
- W2757029003 cites W2015051329 @default.
- W2757029003 cites W2021287651 @default.
- W2757029003 cites W2023858896 @default.
- W2757029003 cites W2025078628 @default.
- W2757029003 cites W2037591273 @default.
- W2757029003 cites W2043651078 @default.
- W2757029003 cites W2047740187 @default.
- W2757029003 cites W2058006650 @default.
- W2757029003 cites W2063099262 @default.
- W2757029003 cites W2078716275 @default.
- W2757029003 cites W2079050196 @default.
- W2757029003 cites W2119683782 @default.
- W2757029003 cites W2128171794 @default.
- W2757029003 cites W2171925512 @default.
- W2757029003 cites W2268066121 @default.
- W2757029003 cites W2409563713 @default.
- W2757029003 cites W2738996050 @default.
- W2757029003 doi "https://doi.org/10.3892/mmr.2017.7580" @default.
- W2757029003 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5865865" @default.
- W2757029003 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/28944894" @default.
- W2757029003 hasPublicationYear "2017" @default.
- W2757029003 type Work @default.
- W2757029003 sameAs 2757029003 @default.
- W2757029003 citedByCount "16" @default.
- W2757029003 countsByYear W27570290032018 @default.
- W2757029003 countsByYear W27570290032019 @default.
- W2757029003 countsByYear W27570290032020 @default.
- W2757029003 countsByYear W27570290032021 @default.
- W2757029003 countsByYear W27570290032022 @default.
- W2757029003 countsByYear W27570290032023 @default.
- W2757029003 crossrefType "journal-article" @default.
- W2757029003 hasAuthorship W2757029003A5000979147 @default.
- W2757029003 hasAuthorship W2757029003A5004641991 @default.
- W2757029003 hasAuthorship W2757029003A5023492006 @default.
- W2757029003 hasAuthorship W2757029003A5032229723 @default.
- W2757029003 hasAuthorship W2757029003A5043185825 @default.
- W2757029003 hasAuthorship W2757029003A5052676364 @default.
- W2757029003 hasAuthorship W2757029003A5060337298 @default.
- W2757029003 hasAuthorship W2757029003A5077471484 @default.
- W2757029003 hasAuthorship W2757029003A5082789515 @default.
- W2757029003 hasBestOaLocation W27570290031 @default.
- W2757029003 hasConcept C153911025 @default.
- W2757029003 hasConcept C190283241 @default.
- W2757029003 hasConcept C22615655 @default.
- W2757029003 hasConcept C2775934118 @default.
- W2757029003 hasConcept C29311851 @default.
- W2757029003 hasConcept C31573885 @default.
- W2757029003 hasConcept C54009773 @default.
- W2757029003 hasConcept C54355233 @default.
- W2757029003 hasConcept C55493867 @default.
- W2757029003 hasConcept C81885089 @default.
- W2757029003 hasConcept C86803240 @default.
- W2757029003 hasConcept C88634738 @default.
- W2757029003 hasConcept C95444343 @default.
- W2757029003 hasConceptScore W2757029003C153911025 @default.
- W2757029003 hasConceptScore W2757029003C190283241 @default.
- W2757029003 hasConceptScore W2757029003C22615655 @default.
- W2757029003 hasConceptScore W2757029003C2775934118 @default.
- W2757029003 hasConceptScore W2757029003C29311851 @default.
- W2757029003 hasConceptScore W2757029003C31573885 @default.
- W2757029003 hasConceptScore W2757029003C54009773 @default.
- W2757029003 hasConceptScore W2757029003C54355233 @default.
- W2757029003 hasConceptScore W2757029003C55493867 @default.
- W2757029003 hasConceptScore W2757029003C81885089 @default.
- W2757029003 hasConceptScore W2757029003C86803240 @default.
- W2757029003 hasConceptScore W2757029003C88634738 @default.
- W2757029003 hasConceptScore W2757029003C95444343 @default.
- W2757029003 hasIssue "5" @default.
- W2757029003 hasLocation W27570290031 @default.
- W2757029003 hasLocation W27570290032 @default.
- W2757029003 hasLocation W27570290033 @default.
- W2757029003 hasLocation W27570290034 @default.
- W2757029003 hasOpenAccess W2757029003 @default.
- W2757029003 hasPrimaryLocation W27570290031 @default.
- W2757029003 hasRelatedWork W2017972840 @default.