ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2018
Rho kinase inhibition maintains intestinal and vascular barrier function by upregulation of occludin in experimental necrotizing enterocolitis.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 33 citations in OpenAlex.
- Tight junction dysfunction and cytoskeletal remodeling in Hirschsprung‑associated enterocolitis: A decade of mechanistic insights and therapeutic prospects (Review).Molecular medicine reports · 2026Review
- Necrotizing Enterocolitis: What's New and What's Next?International journal of molecular sciences · 2025Review
- Inflammatory bowel disease risk gene C1ORF106 regulates actin dynamics in intestinal epithelial cells.bioRxiv : the preprint server for biology · 2025Article
- Role of E-cadherin in epithelial barrier dysfunction: implications for bacterial infection, inflammation, and disease pathogenesis.Frontiers in cellular and infection microbiology · 2025Review
- Berberine alleviates enterotoxigenicFrontiers in nutrition · 2024Article
- Occludin: a gatekeeper of brain Infection by HIV-1.Fluids and barriers of the CNS · 2023Review
- Tight junctions: from molecules to gastrointestinal diseases.Tissue barriers · 2023Article
- Bamboo Shoot andCurrent issues in molecular biology · 2022Article
- Effects of acute and chronic oxidative stress on the blood-brain barrier in 2D and 3D in vitro models.Fluids and barriers of the CNS · 2022Article
- Cadmium exposure enhances VE-cadherin expression in endothelial cells via suppression of ROCK signaling.Experimental and therapeutic medicine · 2022Article
- Understanding the development and function of the gut microbiota in health and inflammation.Frontline gastroenterology · 2022Article
- Experimental Modeling of Necrotizing Enterocolitis in Human Infant Intestinal Enteroids.Journal of investigative surgery : the official journal of the Academy of Surgical Research · 2022Article
- DRG1 Maintains Intestinal Epithelial Cell Junctions and Barrier Function by Regulating RAC1 Activity in Necrotizing Enterocolitis.Digestive diseases and sciences · 2021Article
- Small-molecule modulators of INAVA cytosolic condensate and cell-cell junction assemblies.The Journal of cell biology · 2021Article
- Necrotizing Enterocolitis: Overview on In Vitro Models.International journal of molecular sciences · 2021Review
- Review
- New directions in necrotizing enterocolitis with early-stage investigators.Pediatric research · 2020Review
- ROCK1 inhibitor stabilizes E-cadherin and improves barrier function in experimental necrotizing enterocolitis.American journal of physiology. Gastrointestinal and liver physiology · 2020Article
- Inhibition of AMediators of inflammation · 2020Article
- Recent Advances in Prevention and Therapies for Clinical or Experimental Necrotizing Enterocolitis.Digestive diseases and sciences · 2019Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Necrotizing enterocolitis (NEC) is a deadly disease that occurs in 5-10% of neonates. Although NEC has been extensively studied, no single therapeutic target has been identified. Rho kinase (ROCK) is a serine/threonine kinase that affects multiple cellular processes, including tight junction (TJ) function, cellular permeability, and apoptosis. We hypothesized that ROCK inhibition would decrease cellular permeability, stabilize TJ proteins (occludin), and decrease the severity of NEC. To test this hypothesis, human colon epithelial cells (Caco-2) and human endothelial cells were studied. Cells were treated with lipopolysaccharide to simulate an in vitro model of NEC. The effect of ROCK inhibition was measured by transepithelial membrane resistance (TEER) and cellular permeability to FITC-dextran. The effects of ROCK inhibition in vivo were analyzed in the rat pup model of NEC. NEC was induced by feeding formula supplemented with Cronobacter sakazakii with or without gavaged ROCK inhibitor. Rat intestines were scored based on histological degree of injury. RNA and protein assays for occludin protein were performed for all models of NEC. Treatment with ROCK inhibitor significantly decreased cellular permeability in Caco-2 cells and increased TEER. Intestinal injury scoring revealed decreased scores in ROCK inhibitor-treated pups compared with NEC only. Both cell and rat pup models demonstrated an upregulation of occludin expression in the ROCK inhibitor-treated groups. Therefore, we conclude that ROCK inhibition protects against experimental NEC by strengthening barrier function via upregulation of occludin. These data suggest that ROCK may be a potential therapeutic target for patients with NEC. NEW & NOTEWORTHY These studies are the first to demonstrate an upregulation of occludin tight junction protein in response to Rho kinase (ROCK) inhibition. Furthermore, we have demonstrated that ROCK inhibition in experimental models of necrotizing enterocolitis (NEC) is protective against NEC in both in vitro and in vivo models of disease.
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