Functional role of microRNA-135a in colitis

Lou, Chunyan; Li, Yanyang

doi:10.1186/s12950-018-0181-z

Cited by 9 publications

(5 citation statements)

References 25 publications

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“…In this case, miRNAs complementary antisense oligonucleotides or miRNA mimics can be potential therapeutics that abolish or mimic miRNA’s function and, therefore, block inflammatory progression, modulate cytokines or chemokine hemostasis and increase the treatment sensitivity of conventional therapies. As such, miRNAs are used for modulating hypoxia ( 183 , 184 ) and the inflammatory response by targeting major inflammatory pathways ( 185 – 189 ) and essential molecules, including tight junction proteins that maintain the integrity of the membrane ( 74 , 190 , 191 ).…”

Section: Discussionmentioning

confidence: 99%

Differentially Expressed miRNAs in Ulcerative Colitis and Crohn’s Disease

Yarani

Shojaeian²,

Palasca³

et al. 2022

Front. Immunol.

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Differential microRNA (miRNA or miR) regulation is linked to the development and progress of many diseases, including inflammatory bowel disease (IBD). It is well-established that miRNAs are involved in the differentiation, maturation, and functional control of immune cells. miRNAs modulate inflammatory cascades and affect the extracellular matrix, tight junctions, cellular hemostasis, and microbiota. This review summarizes current knowledge of differentially expressed miRNAs in mucosal tissues and peripheral blood of patients with ulcerative colitis and Crohn’s disease. We combined comprehensive literature curation with computational meta-analysis of publicly available high-throughput datasets to obtain a consensus set of miRNAs consistently differentially expressed in mucosal tissues. We further describe the role of the most relevant differentially expressed miRNAs in IBD, extract their potential targets involved in IBD, and highlight their diagnostic and therapeutic potential for future investigations.

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Section: Discussionmentioning

confidence: 99%

Differentially Expressed miRNAs in Ulcerative Colitis and Crohn’s Disease

Yarani

Shojaeian²,

Palasca³

et al. 2022

Front. Immunol.

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“…Furthermore, the authors showed that HIF-1α is a target of miR-135a, and that the downregulation of miR-135a enhances HIF-1α expression to promote apoptosis and inflammation. Consistently, the overexpression of miR-135a in colonic epithelial cells prevented apoptosis and inflammation by inhibiting the expression of apoptotic factor Bax and enhancing the expression of anti-apoptotic factor Bcl-2 via HIF-1α [ 131 ]. Another study found a negative correlation between miR-16 and Bcl-2 expression in Caco-2 cells and in the colonic mucosa of DSS-treated mice [ 107 ].…”

Section: Microrna As a Therapeutic Target In Ibdmentioning

confidence: 98%

“…miR-135a was found to be suppressed in both UC and CD patients [ 86 ]. Lou et al [ 131 ] showed that the DSS model (4% DSS) recapitulates human colitis and results in the significant downregulation of miR-135a. Furthermore, the authors showed that HIF-1α is a target of miR-135a, and that the downregulation of miR-135a enhances HIF-1α expression to promote apoptosis and inflammation.…”

Section: Microrna As a Therapeutic Target In Ibdmentioning

confidence: 99%

Role of MicroRNA in Inflammatory Bowel Disease: Clinical Evidence and the Development of Preclinical Animal Models

Suri

Bubier

Wiles

et al. 2021

Cells

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The dysregulation of microRNA (miRNA) is implicated in cancer, inflammation, cardiovascular disorders, drug resistance, and aging. While most researchers study miRNA’s role as a biomarker, for example, to distinguish between various sub-forms or stages of a given disease of interest, research is also ongoing to utilize these small nucleic acids as therapeutics. An example of a common pleiotropic disease that could benefit from miRNA-based therapeutics is inflammatory bowel disease (IBD), which is characterized by chronic inflammation of the small and large intestines. Due to complex interactions between multiple factors in the etiology of IBD, development of therapies that effectively maintain remission for this disease is a significant challenge. In this review, we discuss the role of dysregulated miRNA expression in the context of clinical ulcerative colitis (UC) and Crohn’s disease (CD)—the two main forms of IBD—and the various preclinical mouse models of IBD utilized to validate the therapeutic potential of targeting these miRNA. Additionally, we highlight advances in the development of genetically engineered animal models that recapitulate clinical miRNA expression and provide powerful preclinical models to assess the diagnostic and therapeutic promise of miRNA in IBD.

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“…MiR-26a targeted to regulate hepatocyte growth factor (HGF), and then affect hgfcmet signal, angiogenesis and metastasis (17)(18)(19). Tgf-mir-34a-ccl22 axis causes accumulation of T cells regulated by portal vein system, destroys immune microenvironment, and leads to proliferation and vascular metastasis of scattered tumor cells (20)(21)(22). LncRNA can interact with DNA, RNA and protein to realize the diversification of its functions (23).…”

Section: Introductionmentioning

confidence: 99%

Mir 135a inhibits tumor cell proliferation by regulating the expression of notch pathway in hepatoblastoma

Zhao

Chen

et al. 2022

Cell Mol Biol (Noisy-le-grand)

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MiRNA affects the proliferation, migration and cycle of tumor cells. However, the mechanism of regulating Notch pathway expression and inhibiting tumor cell proliferation in hepatoblastoma is not clear, we need to further explore. In this study, the dact2 gene can inhibit liver fibrosis. In this experiment, we used in vitro culture of hepatoblastoma cells and flow cytometry to detect the effect of miRNA-135a on the tumor cell cycle. The expression of miRNA-135a was detected by real-time PCR in 6 tumor samples and normal controls to observe and analyze the expression level of the important signal pathway proteins in the cells after mir-135a transfection. The cells were divided into the experimental group and the control group. The experimental group was transfected with miRNA-135a cells, while the control group was not transfected. Finally, the data are analyzed and discussed. from the third day, the activity of M17 cells in the mir-135a group began to be inhibited. By the fifth day, the inhibition rate of M17 was 50.64% (P < 0.01), and M21 was 25.02% (P < 0.01). In the experimental group, 53.38% of the cells were in the G1 phase, and mir-135a could block the tumor cells in G1 phase, affect the cell cycle process, and then affect cell proliferation.

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Functional role of microRNA-135a in colitis

Cited by 9 publications

References 25 publications

Differentially Expressed miRNAs in Ulcerative Colitis and Crohn’s Disease

Differentially Expressed miRNAs in Ulcerative Colitis and Crohn’s Disease

Role of MicroRNA in Inflammatory Bowel Disease: Clinical Evidence and the Development of Preclinical Animal Models

Mir 135a inhibits tumor cell proliferation by regulating the expression of notch pathway in hepatoblastoma

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