MicroRNA-590-5p Inhibits Intestinal Inflammation by Targeting YAP

Yu, Minhao; Luo, Yang; Cong, Zhi-Jie; Mu, Yi-Fei; Qiu, Yier; Zhong, Ming

doi:10.1093/ecco-jcc/jjy046

Cited by 41 publications

(25 citation statements)

References 46 publications

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“…In particular, previous literature has reported that YAP is crucial for epithelial progenitor cell proliferation and differentiation, and is involved in epithelial repair 123 . YAP mRNA is significantly upregulated in IECs in patients with CD and mice with colitis 47 . In the DSS-induced colitis and regeneration models, YAP is overexpressed and colonic epithelial cells in crypts actively proliferate 8,43 .…”

Section: Hippo and The Pathophysiology Of Ibd-associated Colitis Hippmentioning

confidence: 97%

“…Increasing research in recent years has indicated an interplay between the Hippo and other pathways in intestinal regeneration, including the WNT 43 and Notch 44 pathway. Furthermore, the Hippo pathway has been suggested to be associated with inflammation, including the NF-κB pathways 45,46 and other components 9,47 , and also with immune-regulating pathways 15 .…”

Section: Interplays Between the Hippo Signalling And Other Pathwaysmentioning

confidence: 99%

“…Activation of YAP/TAZ has been revealed to promote intestinal tissue repair and colonic regeneration in a mouse DSS colitis model via the extracellular matrix (ECM) remodelling and FAK/Src signalling activation, and ultimately reprograms the epithelium transiently into a primitive state, where the ISCs play an extremely important role 122 . Importantly, YAP/TAZ promote cellular proliferation via transcription of TEADs in the gut epithelium, especially in ISCs 47 . In particular, previous literature has reported that YAP is crucial for epithelial progenitor cell proliferation and differentiation, and is involved in epithelial repair 123 .…”

Section: Hippo and The Pathophysiology Of Ibd-associated Colitis Hippmentioning

confidence: 99%

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The role of the Hippo pathway in the pathogenesis of inflammatory bowel disease

et al. 2021

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Inflammatory bowel disease (IBD) is a chronic and recurrent inflammatory disorder that primarily comprises Crohn’s disease (CD) and ulcerative colitis (UC). Owing to its increasing prevalence in Eastern countries and the intractable challenges faced during IBD treatment, extensive research on IBD has been carried out over the last few years. Although the precise aetiology of IBD is undefined, the currently accepted hypothesis for IBD pathogenesis considers it to be a combination of environment, genetic predisposition, gut microbiota, and abnormal immunity. A recently emerged signalling pathway, the Hippo pathway, acts as a key regulator of cell growth, tissue homoeostasis, organ size, and has been implicated in several human cancers. In the past few years, studies have revealed the importance of the Hippo pathway in gastrointestinal tract physiology and gastrointestinal diseases, such as colorectal cancer and IBD. However, the role of the Hippo pathway and its exact impact in IBD remains to be elucidated. This review summarises the latest scientific literature on the involvement of this pathway in IBD from the following perspectives that account for the IBD pathogenesis: intestinal epithelial cell regeneration, immune regulation, gut microbiota, and angiogenesis. A comprehensive understanding of the specific role of the Hippo pathway in IBD will provide novel insights into future research directions and clinical implications of the Hippo pathway.

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Section: Hippo and The Pathophysiology Of Ibd-associated Colitis Hippmentioning

confidence: 97%

Section: Interplays Between the Hippo Signalling And Other Pathwaysmentioning

confidence: 99%

Section: Hippo and The Pathophysiology Of Ibd-associated Colitis Hippmentioning

confidence: 99%

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The role of the Hippo pathway in the pathogenesis of inflammatory bowel disease

et al. 2021

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“…miR-590-5p was described as part of a six-miRNA panel that reflects the response to chemoradiotherapy (48). One target of the miR-590-5p is Yes associated protein (YAP) (49), which induces cell growth and invasion in BC (50). Overexpression of YAP is partly responsible for poor prognosis in BC (50,51).…”

Section: Validation Cohort N=36 -------------------------------------mentioning

confidence: 99%

Plasma miR‑15b‑5p and miR‑590‑5p for distinguishing patients with bladder cancer from healthy individuals

2019

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MicroRNAs (miRNAs/miRs) act as markers for various cancers, including bladder cancer (BC). Plasma miRNAs are potential biomarkers for the noninvasive diagnosis and long-term surveillance of BC. The aim of the present study was to identify diagnostically reliable miRNAs in the plasma and examine their potential monitoring capacity. miRNAs were measured by reverse transcription-quantitative polymerase chain reaction. The study was performed as a discovery phase, which included plasma samples from each of the 10 patients with and without BC prior to transurethral resection (TURB). The results were validated in a second phase, involving 36 patients with plasma samples collected before the second TURB or radical cystectomy (RC), and after RC. During the discovery step, three elevated miRNAs (miR-15b-5p, miR-590-5p, miR-29b-3p) and two decreased miRNAs (miR-10b-5p, miR-144-5p) were selected as potential miRNA candidates for further validation. miR-15b-5p and miR-590-5p were finally confirmed to discriminate between cancer cases and controls; however, for disease monitoring of BC, both miRNAs were not suitable as a decline in the miRNA levels was not observed in some patients after tumor removal. Our results suggested that circulating miR-15b-5p and miR-590-5p have useful diagnostic potential for BC, but are rather unsuitable as monitoring markers for disease. The reasons of this apparent contradictory observation may be due to the aspect of biological variation of circulating miRNAs and serial measurements could be unreliable.

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“…6 Increasing evidence suggests that miRNAs are widely dysregulated in UC, potentially impacting UC pathogenesis, diagnosis and therapy. [6][7][8] For example, Wu et al found that miR-206 regulates TNF-α and IL-8 in active human UC and dextran sodium sulphate (DSS)-induced experimental colitis in mice. 8 Min et al illustrated that miR-155 overexpression enhanced UC inflammatory activity by down-regulating the expression of FOXO3a, a key inhibitor of the NF-κB signalling pathways.…”

Section: Introductionmentioning

confidence: 99%