Long Noncoding RNA FBXL19-AS1-Mediated Ulcerative Colitis-Associated Intestinal Epithelial Barrier Defect

Xiu-ling, Zhao; Cui, Dejun; Yang, Liu-chan; Yuan, Wenqiang; Yan, F.

doi:10.1007/s13770-022-00479-9

Cited by 7 publications

(4 citation statements)

References 41 publications

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“…Similar to neutrophils, macrophages also produce and secrete various ECM-degrading enzymes (Sutherland et al, 2023). In addition, macrophages ingest and degrade ECM structures by integrin-mediated phagocytosis and receptor-mediated endocytosis (McKleroy et al, 2013;Zhao et al, 2022). On the other hand, macrophages also secrete ECM proteins including fibronectin, laminin and versican, which can help to provide a mechanical scaffold following injury and aid in the renewal of tissue architecture (Tomlin and Piccinini, 2018).…”

Section: Epithelial Barrier Disruption Leads To Inflammation and Loca...mentioning

confidence: 99%

“…Genome-wide association studies (GWAS) have indicated risk alleles in IBD patients in genes involved in intestinal cell restitution (ERRFI1, PTGER4 or HNF4), in cell polarity (PARD3) or in intercellular junctions (MYO9B, MAGI2, GNAI2, LAMB1 or CDH1) (McCole, 2014). At a epigenetic level, long non coding RNA (ncRNA) CCAT1 and FBXL19-AS1 (Ma et al, 2019;Zhao et al, 2022), circular CDKN2B-AS1 and SMAD4 (Rankin et al, 2019;Zhao et al, 2023) and microRNAs (miR) miR-21, miR23a, miR-182-5p (Shi et al, 2013;Yang et al, 2013;Felwick et al, 2020;Xu et al, 2022) overexpression can increase the degradation of the epithelial barrier while miR-195-5p reduces the permeability (Scalavino et al, 2022).…”

Section: Introductionmentioning

confidence: 99%

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Epithelial Barrier Dysfunction in Disease

Pardo-Pastor,

López Posadas,

Ortiz Zapater

2024

Frontiers Research Topics

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Frontiers is more than just an open access publisher of scholarly articles: it is a pioneering approach to the world of academia, radically improving the way scholarly research is managed. The grand vision of Frontiers is a world where all people have an equal opportunity to seek, share and generate knowledge. Frontiers provides immediate and permanent online open access to all its publications, but this alone is not enough to realize our grand goals. Frontiers journal seriesThe Frontiers journal series is a multi-tier and interdisciplinary set of openaccess, online journals, promising a paradigm shift from the current review, selection and dissemination processes in academic publishing. All Frontiers journals are driven by researchers for researchers; therefore, they constitute a service to the scholarly community. At the same time, the Frontiers journal series operates on a revolutionary invention, the tiered publishing system, initially addressing specific communities of scholars, and gradually climbing up to broader public understanding, thus serving the interests of the lay society, too. Dedication to qualityEach Frontiers article is a landmark of the highest quality, thanks to genuinely collaborative interactions between authors and review editors, who include some of the world's best academicians. Research must be certified by peers before entering a stream of knowledge that may eventually reach the public -and shape society; therefore, Frontiers only applies the most rigorous and unbiased reviews. Frontiers revolutionizes research publishing by freely delivering the most outstanding research, evaluated with no bias from both the academic and social point of view. By applying the most advanced information technologies, Frontiers is catapulting scholarly publishing into a new generation. What are Frontiers Research Topics?Frontiers Research Topics are very popular trademarks of the Frontiers journals series: they are collections of at least ten articles, all centered on a particular subject. With their unique mix of varied contributions from Original Research to Review Articles, Frontiers Research Topics unify the most influential researchers, the latest key findings and historical advances in a hot research area.

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Section: Epithelial Barrier Disruption Leads To Inflammation and Loca...mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Epithelial Barrier Dysfunction in Disease

Pardo-Pastor,

López Posadas,

Ortiz Zapater

2024

Frontiers Research Topics

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“…Musas-1 is a neural RNA-binding protein but has been shown to be a selective marker of ISCs in addition to the nervous system[ 18 ]. Some studies found that Musashi-1-positive cells were found in the small intestine of mice, and Musashi-1 was significantly increased in intestinal specimens of mice after reflex injury[ 19 ]. TERT is a ribonuclear protease complex.…”

Section: Repair Mechanism Of Iscs On Intestinal Mucosamentioning

confidence: 99%

Molecular regulation mechanism of intestinal stem cells in mucosal injury and repair in ulcerative colitis

Zheng¹,

Duan²

2023

World J Gastroenterol

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Ulcerative colitis (UC) is a chronic nonspecific inflammatory disease with complex causes. The main pathological changes were intestinal mucosal injury. Leucine-rich repeat-containing G protein coupled receptor 5 (LGR5)-labeled small intestine stem cells (ISCs) were located at the bottom of the small intestine recess and inlaid among Paneth cells. LGR5+ small ISCs are active proliferative adult stem cells, and their self-renewal, proliferation and differentiation disorders are closely related to the occurrence of intestinal inflammatory diseases. The Notch signaling pathway and Wnt/β-catenin signaling pathway are important regulators of LGR5-positive ISCs and together maintain the function of LGR5-positive ISCs. More importantly, the surviving stem cells after intestinal mucosal injury accelerate division, restore the number of stem cells, multiply and differentiate into mature intestinal epithelial cells, and repair the damaged intestinal mucosa. Therefore, in-depth study of multiple pathways and transplantation of LGR5-positive ISCs may become a new target for the treatment of UC.

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“…Genome-wide association studies (GWAS) have indicated risk alleles in IBD patients in genes involved in intestinal cell restitution (ERRFI1, PTGER4 or HNF4), in cell polarity (PARD3) or in intercellular junctions (MYO9B, MAGI2, GNAI2, LAMB1 or CDH1) ( McCole, 2014 ). At a epigenetic level, long non coding RNA (ncRNA) CCAT1 and FBXL19-AS1 ( Ma et al, 2019 ; Zhao et al, 2022 ), circular CDKN2B-AS1 and SMAD4 ( Rankin et al, 2019 ; Zhao et al, 2023 ) and microRNAs (miR) miR-21, miR23a, miR-182-5p ( Shi et al, 2013 ; Yang et al, 2013 ; Felwick et al, 2020 ; Xu et al, 2022 ) overexpression can increase the degradation of the epithelial barrier while miR-195-5p reduces the permeability ( Scalavino et al, 2022 ).…”

Section: A Brief Outline Of the Epithelial Barrier Role In The Pathop...mentioning

confidence: 99%

Role of the epithelial barrier in intestinal fibrosis associated with inflammatory bowel disease: relevance of the epithelial-to mesenchymal transition

Macias-Ceja,

Mendoza-Ballesteros,

Ortega-Albiach

et al. 2023

Front. Cell Dev. Biol.

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In inflammatory bowel disease (IBD), chronic inflammation in the gastrointestinal tract can lead to tissue damage and remodelling, which can ultimately result in fibrosis. Prolonged injury and inflammation can trigger the activation of fibroblasts and extracellular matrix (ECM) components. As fibrosis progresses, the tissue becomes increasingly stiff and less functional, which can lead to complications such as intestinal strictures, obstructive symptoms, and eventually, organ dysfunction. Epithelial cells play a key role in fibrosis, as they secrete cytokines and growth factors that promote fibroblast activation and ECM deposition. Additionally, epithelial cells can undergo a process called epithelial-mesenchymal transition, in which they acquire a more mesenchymal-like phenotype and contribute directly to fibroblast activation and ECM deposition. Overall, the interactions between epithelial cells, immune cells, and fibroblasts play a critical role in the development and progression of fibrosis in IBD. Understanding these complex interactions may provide new targets for therapeutic interventions to prevent or treat fibrosis in IBD. In this review, we have collected and discussed the recent literature highlighting the contribution of epithelial cells to the pathogenesis of the fibrotic complications of IBD, including evidence of EMT, the epigenetic control of the EMT, the potential influence of the intestinal microbiome in EMT, and the possible therapeutic strategies to target EMT. Finally we discuss the pro-fibrotic interactions epithelial-immune cells and epithelial-fibroblasts cells.

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Long Noncoding RNA FBXL19-AS1-Mediated Ulcerative Colitis-Associated Intestinal Epithelial Barrier Defect

Cited by 7 publications

References 41 publications

Epithelial Barrier Dysfunction in Disease

Epithelial Barrier Dysfunction in Disease

Molecular regulation mechanism of intestinal stem cells in mucosal injury and repair in ulcerative colitis

Role of the epithelial barrier in intestinal fibrosis associated with inflammatory bowel disease: relevance of the epithelial-to mesenchymal transition

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