ArticleMedical science monitor : international medical journal of experimental and clinical research2018
Rho Kinase Type 1 (ROCK1) Promotes Lipopolysaccharide-induced Inflammation in Corneal Epithelial Cells by Activating Toll-Like Receptor 4 (TLR4)-Mediated Signaling.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 27 citations in OpenAlex.
- Infosomes as Inflammatory Mediators: Proteomic Profiling of Proteins Enriched in Inflammatory Extracellular Vesicles.Molecular & cellular proteomics : MCP · 2026Article
- Evaluation of cytotoxicity, wound healing, and anti-inflammatory effects of netarsudil on human corneal epithelial cells.Scientific reports · 2026Article
- Butyric acid and valeric acid attenuate stress-induced ferroptosis and depressive-like behaviors by suppressing hippocampal neuroinflammation.Journal of translational medicine · 2025Article
- A Comprehensive Review of the Role of Rho-Kinase Inhibitors in Corneal Diseases.Life (Basel, Switzerland) · 2025Review
- Rnd3 suppresses endothelial cell pyroptosis in atherosclerosis through regulation of ubiquitination of TRAF6.Clinical and translational medicine · 2023Article
- 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
- MicroRNA‑502‑3p promotesMolecular medicine reports · 2021Article
- Protective effects of dexmedetomidine on cerebral ischemia/reperfusion injury via the microRNA-214/ROCK1/NF-κB axis.BMC anesthesiology · 2021Article
- Effects of ROCK Inhibitors on Apoptosis of Corneal Endothelial Cells in CMV-Positive Posner-Schlossman Syndrome Patients.Investigative ophthalmology & visual science · 2020Article
- Oral l-Cysteine Supplementation Enhances the Long Term-Effect of Topical Basic Fibroblast Growth Factor (bFGF) in Reducing the Corneal Haze after Photorefractive Keratectomy in Myopic Patients.Pharmaceuticals (Basel, Switzerland) · 2020Article
- JNK Signaling as a Key Modulator of Soft Connective Tissue Physiology, Pathology, and Healing.International journal of molecular sciences · 2020Review
- Dysregulation of miR-202-3p Affects Migration and Invasion of Endometrial Stromal Cells in Endometriosis via Targeting ROCK1.Reproductive sciences (Thousand Oaks, Calif.) · 2020Article
- Down-Regulation of circNRIP1 Promotes the Apoptosis and Inhibits the Migration and Invasion of Gastric Cancer Cells by miR-182/ROCK1 Axis.OncoTargets and therapy · 2020Article
- Molecular regulation of TLR signaling in health and disease: mechano-regulation of macrophages and TLR signaling.Innate immunity · 2020Review
- Review
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND Rho kinases (ROCKs) are the typical downstream effectors of RhoA, which can regulate corneal epithelial wound healing. In this study, the role of ROCK1 in lipopolysaccharide (LPS)-induced cornea inflammation was investigated. MATERIAL AND METHODS The expression of ROCK1 in human corneal epithelial cells (HCECs) was bilaterally modulated with ROCK1 expression vector and ROCK1 inhibitor Y-27632. The effects of ROCK1 modulation on the inflammatory response, cell viability, cell apoptosis, and cell cycle distribution were detected by ELISA assay, MTT assay, and flow cytometry, respectively. The pathways involved in the effect of ROCK1 in HCECs was preliminarily explained by detecting changes of TLR4-mediated NF-kB and ERK signaling using western blotting and electrophoretic mobility shift assays. RESULTS Overexpression of ROCK1 promoted LPS-induced production of IL-6, IL-8, IL-1β, and TNF-α, and the apoptotic process in HCECs. Augmented inflammation and apoptosis were associated with stronger activation of TLR4-mediated signal transduction; the phosphorylation of IkBa, JNK, ERK1/2, and p38, and nuclear translocation of NF-κB p65 induced by LPS were further increased by overexpression of ROCK1. Inhibition of ROCK1 function by Y-27632 blocked the effect of LPS on HCECs; both LPS-induced inflammation and apoptosis was alleviated by Y-27632, which was associated with suppression of TLR4-mediated NF-κB and ERK signaling. CONCLUSIONS LPS-induced inflammation and apoptosis in HCECs depended on the function of ROCK1, inhibition of which would attenuate impairments on cornea cells due to LPS.
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