ArticleThe Journal of international medical research2021
Lnc-NEAT1 induces cell apoptosis and inflammation but inhibits proliferation in a cellular model of hepatic ischemia/reperfusion injury.
Article in The Journal of international medical research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- Evaluation of serum NEAT1 and MALAT1 expression as diagnostic biomarkers in tyrosinemia, a rare metabolic disorder.Orphanet journal of rare diseases · 2026Article
- Non-coding RNAs: The potential biomarker or therapeutic target in hepatic ischemia-reperfusion injury.World journal of gastroenterology · 2023Review
- Silencing lncRNA KCNQ1OT1 reduced hepatic ischemia reperfusion injury-induced pyroptosis by regulating miR-142a-3p/HMGB1 axis.Molecular and cellular biochemistry · 2023Article
- lncRNA DHFRL1‑4 knockdown attenuates cerebral ischemia/reperfusion injury by upregulating the levels of angiogenesis‑related genes.International journal of molecular medicine · 2022Article
- LncRNA NEAT1 correlates with Th17 cells and proinflammatory cytokines, also reflects stenosis degree and cholesterol level in coronary heart disease patients.Journal of clinical laboratory analysis · 2022Article
- Aberrant expressions of circulating lncRNA NEAT1 and microRNA-125a are linked with Th2 cells and symptom severity in pediatric allergic rhinitis.Journal of clinical laboratory analysis · 2022Article
- Novel Insights into the Emerging Role of Neat1 and Its Effects Downstream in the Regulation of Inflammation.Journal of inflammation research · 2022Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveWe aimed to investigate the effect of long non-coding RNA nuclear-enriched abundant transcript 1 (lnc-NEAT1) on regulating hepatocyte proliferation, apoptosis, and inflammation during hepatic ischemia/reperfusion (I/R) injury.
methodsHuman liver cells (HL-7702) were cultured under glucose-free and oxygen-free conditions to construct the I/R injury model. Expression of lnc-NEAT1 was detected in this model and in normal cells. Plasmids of control overexpression [NC(+)], lnc-NEAT1 overexpression [NEAT1(+)], control short hairpin (sh)RNA [NC(-)], and lnc-NEAT1 shRNA [NEAT1(-)] were transfected into HL-7702 cells and subsequently subjected to I/R treatment. Cell proliferation, apoptosis, apoptosis-related proteins, and inflammatory cytokines were assessed.
resultsLnc-NEAT1 expression was elevated in the I/R group compared with the normal group. Cell proliferation was decreased in the NEAT1(+) group compared with the NC(+) group but increased in NEAT1(-) compared with NC(-). The apoptosis rate increased in the NEAT1(+) group compared with the NC(+) group but decreased in NEAT1(-) compared with NC(-). Western blot assay (detection of apoptosis-related proteins) showed similar results. Expression of interleukin-1β, interleukin-6, and tumor necrosis factor-α increased in the NEAT1(+) group compared with NC(+) but decreased in NEAT1(-) compared with NC(-).
conclusionLnc-NEAT1 is overexpressed, induces cell apoptosis and inflammation, and inhibits proliferation during hepatic I/R injury.
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