ArticleThe Kaohsiung journal of medical sciences2020
miR-495 targets ROCK1 to inhibit lipopolysaccharides-induced WI-38 cells apoptosis and inflammation.
Article in The Kaohsiung journal of medical sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 13 citations in OpenAlex.
- Vitexin mitigates oxidative stress, mitochondrial damage, pyroptosis and regulates small nucleolar RNA host gene 1/DNA methyltransferase 1/microRNA-495 axis in sepsis-associated acute lung injury.Inflammopharmacology · 2025Article
- Reduced Expression of miR-146a Potentiates Intestinal Inflammation following Alcohol and Burn Injury.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- lncRNA NEAT1 mediates LPS-induced pyroptosis of BEAS-2B cells via targeting miR-26a-5p/ROCK1 axis.The Kaohsiung journal of medical sciences · 2023Article
- Implication of non-coding RNA-mediated ROCK1 regulation in various diseases.Frontiers in molecular biosciences · 2022Review
- Article
- Knockdown of lncRNA LUCAT1 attenuates sepsis‑induced myocardial cell injury by sponging miR-642a.Mammalian genome : official journal of the International Mammalian Genome Society · 2021Article
- Long non-coding RNA colorectal neoplasia differentially expressed correlates negatively with miR-33a and miR-495 and positively with inflammatory cytokines in asthmatic children.The clinical respiratory journal · 2021Article
- Circ_0114428 Regulates Sepsis-Induced Kidney Injury by Targeting the miR-495-3p/CRBN Axis.Inflammation · 2021Article
- Transcriptomic Analysis Exploring the Molecular Mechanisms of Hanchuan Zupa Granules in Alleviating Asthma in Rat.Evidence-based complementary and alternative medicine : eCAM · 2021Article
- miR-495 targets ROCK1 to inhibit lipopolysaccharides-induced WI-38 cells apoptosis and inflammation.The Kaohsiung journal of medical sciences · 2020Article
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Authors and funding
6 authors at 2 institutions in 1 country.
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Abstract
Pneumonia is an inflammatory disease with leading mortality rate in children. It has been well established that microRNAs (miRNAs) have been regarded as critical regulator in acute lung injury. We intended to explore the effect and underlying mechanism of miR-495 on lipopolysaccharides (LPS)-induced WI-38 cells. Here, we first found that miR-495 was downregulated in serum of patients with acute stage pneumonia. To establish cell model of acute pneumonia, WI-38 cells were treated with 20 μg/mL LPS, and qRT-PCR analysis also confirmed the downregulation of miR-495 in LPS-induced WI-38 cells. Data from MTT (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide) and flow cytometry assays showed that the decreased cell viability and induced cell apoptosis by LPS treatment were also reversed by miR-495 over-expression. Moreover, miR-495 inhibited expression of associated inflammatory factors, which were induced by LPS treatment. Second, ROCK1 (rho-associated, coiled-coil-containing protein kinase 1) was identified as functional target gene of miR-495, whose expression was decreased by miR-495. Mechanically, combination of miR-495 and ROCK1 over-expression reversed the influence of miR-495 on LPS-induced inflammation, viability, and apoptosis. In conclusion, our findings indicated that miR-495 inhibited LPS-induced inflammation injury and apoptosis in WI-38 cells via targeting ROCK1, which would shed light on therapeutic schedule in acute pneumonia.
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