ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2020
ROCK1 inhibitor stabilizes E-cadherin and improves barrier function in experimental necrotizing enterocolitis.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 26 citations in OpenAlex.
- The RNA-binding protein Imp1 promotes a Spdef transcriptional program and mucus fucosylation during necrotizing enterocolitis.American journal of physiology. Gastrointestinal and liver physiology · 2026Article
- Necrotizing enterocolitis.Nature reviews. Disease primers · 2026Review
- The RNA-binding protein Imp1 promotes a Spdef transcriptional program and mucus fucosylation during necrotizing enterocolitis.bioRxiv : the preprint server for biology · 2026Article
- The Novel ROCK Inhibitor Fasudil Derivative Fasudil-D-6h Prevents Tumour Progression by Regulating the Adherens Junction Signalling Pathway in Triple-Negative Breast Cancer.Breast cancer (Dove Medical Press) · 2026Article
- Review: microbial metabolites - a key to address gut inflammation and barrier dysfunction in the premature infant.Gut microbes · 2025Review
- Maternal Western diet increases inflammatory markers and decreases barrier function of offspring inAmerican journal of physiology. Gastrointestinal and liver physiology · 2025Article
- MicroRNA-microbiota interactions: Emerging strategies for modulating intestinal homeostasis and enhancing host health.iMetaOmics · 2025Review
- N6-methyladenosine (m6A) RNA methylation of LncRNA LINC01214 accelerates the progression of non-small cell lung cancer (NSCLC) by targeting miR-195-5p/ROCK1 axis.Cytotechnology · 2025Article
- Article
- Glutaredoxin-1 modulates the NF-κB signaling pathway to activate inducible nitric oxide synthase in experimental necrotizing enterocolitis.Molecular therapy. Methods & clinical development · 2024Article
- The Analysis of Embryoid Body Formation and Its Role in Retinal Organoid Development.International journal of molecular sciences · 2024Article
- Novel Histone Deacetylase 6 Inhibitor Confers Anti-inflammatory Effects and Enhances Gut Barrier Function.Gut and liver · 2023Article
- Multiple pathways promote microtubule stabilization in senescent intestinal epithelial cells.npj aging · 2022Article
- In Vitro Apical-Out Enteroid Model of Necrotizing Enterocolitis.Journal of visualized experiments : JoVE · 2022Article
- Understanding the development and function of the gut microbiota in health and inflammation.Frontline gastroenterology · 2022Article
- Artemisinin analog SM934 alleviates epithelial barrier dysfunctionFrontiers in pharmacology · 2022Article
- DRG1 Maintains Intestinal Epithelial Cell Junctions and Barrier Function by Regulating RAC1 Activity in Necrotizing Enterocolitis.Digestive diseases and sciences · 2021Article
- Article
- Review
- Microtissue Geometry and Cell-Generated Forces Drive Patterning of Liver Progenitor Cell Differentiation in 3D.Advanced healthcare materials · 2021Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Necrotizing enterocolitis (NEC) is a devastating gastrointestinal disease of newborns. Although incompletely understood, NEC is associated with intestinal barrier dysfunction. E-cadherin, an adherens junction, is a protein complex integral in maintaining normal barrier homeostasis. Rho-associated protein kinase-1 (ROCK1) is a kinase that regulates the E-cadherin complex, and p120-catenin is a subunit of the E-cadherin complex that has been implicated in stabilizing the cadherin complex at the plasma membrane. We hypothesized that E-cadherin is decreased in NEC and that inhibition of ROCK1 would protect against adherens junction disruption. To investigate this, a multimodal approach was used: In vitro Caco-2 model of NEC (LPS/TNFα), rap pup model (hypoxia + bacteria-containing formula), and human intestinal samples. E-cadherin was decreased in NEC compared with controls, with relocalization from the cell border to an intracellular location. ROCK1 exhibited a time-dependent response to disease, with increased early expression in NEC and decreased expression at later time points and disease severity. Administration of ROCK1 inhibitor (RI) resulted in preservation of E-cadherin expression at the cell border, preservation of intestinal villi on histological examination, and decreased apoptosis. ROCK1 upregulation in NEC led to decreased association of E-cadherin to p120 and increased intestinal permeability. RI helped maintain the stability of the E-cadherin-p120 complex, leading to improved barrier integrity and protection from experimental NEC.
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