MCL-1 is modulated in Crohn’s disease fibrosis by miR-29b via IL-6 and IL-8

Nijhuis, Anke; Curciarello, Renata; Mehta, Shameer; Feakins, Roger; Bishop, Cleo L.; Lindsay, James O.; Silver, Andrew

doi:10.1007/s00441-017-2576-1

Cited by 29 publications

(24 citation statements)

References 47 publications

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“…Among the selected methylation sites, C7orf72 18 and HLA-DRB1 19 had been confirmed to be related to CD by GWAS. As mentioned previously, MUC1 35 – 38 and YPEL5 39 were genes involved in the process of apoptosis, which proved that CD penetrating intestinal mucosal lesions were related to apoptosis. Methylation abnormalities in MUC1 also suggested that CD penetrating intestinal mucosal lesions were associated with ECM abnormalities.…”

Section: Discussionsupporting

confidence: 67%

“…Interestingly, the MUC1 expression in CD was reduced in earlier studies 33 , 34 . In addition, studies 35 – 38 had confirmed that MUC1 was confirmed to be involved in multiple apoptosis signaling pathways.…”

Section: Discussionmentioning

confidence: 96%

“…The secretion of IL-8 in CD was also significantly increased 45 , 46 , and some studies 47 had used it as a biomarker. IL-8 and MUC1 were both important factors involved in the pathophysiological process of CD 28 , 38 .…”

Section: Discussionmentioning

confidence: 98%

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Intestinal mucosa-derived DNA methylation signatures in the penetrating intestinal mucosal lesions of Crohn’s disease

Wang

et al. 2021

Sci Rep

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The purpose of this study was to evaluate genome-wide DNA methylation changes in intestinal mucosa tissue of adult patients with Crohn's disease comprehensively. DNA methylation chip was used to analyze abnormal methylation sites among penetrating and non-penetrating intestinal mucosa tissue of Crohn's disease and normal intestinal mucosa tissue of healthy controls. Methylation abnormalities of different locus were verified by pyrosequencing and quantitative polymerase chain reaction. Differential DNA methylation sites were participated in the positive regulation of apoptosis and the positive regulation of IL-8 production and were enriched in signaling pathways related to inflammatory bowel disease and extracellular matrix receptor interaction signaling pathways. Correlation analysis showed that the methylation abnormalities of HLA-DRB1 (r = − 0.62, P < 0.001), MUC1 (r = − 0.45, P = 0.01), YPEL5 (r = − 0.55, P = 0.001) and CBLB (r = − 0.62, P < 0.001) were significantly negatively correlated with their relative expression levels. The degree of methylation abnormality of MUC1 was negatively correlated with the disease activity score of Crohn's disease (r = − 0.50, P = 0.01). Apoptosis, interleukin-8 production and abnormal extracellular matrix might be involved in the mechanism of penetrating intestinal mucosal lesions in Crohn's disease. The degree of abnormal methylation of MUC1 was negatively correlated with the disease activity of Crohn's disease.

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Section: Discussionsupporting

confidence: 67%

Section: Discussionmentioning

confidence: 96%

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Intestinal mucosa-derived DNA methylation signatures in the penetrating intestinal mucosal lesions of Crohn’s disease

Wang

et al. 2021

Sci Rep

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“…The up-regulated IL21R also suggested B cell maturation, since the B cell differentiation required direct IL21R signals (King et al, 2010 ). In addition, the down-regulated MCL1 mediated by miR-429b suggested that there was a weakening in MCL1's protection from epithelial apoptosis (Lv et al, 2014 ; Nijhuis et al, 2017 ). This was in accordance with the finding that SBM diet increased turnover of intestinal epithelial cells (Chikwati et al, 2013 ).…”

Section: Discussionmentioning

confidence: 99%

Integrative Transcriptomic and microRNAomic Profiling Reveals Immune Mechanism for the Resilience to Soybean Meal Stress in Fish Gut and Liver

Wang

Cui

et al. 2018

Front. Physiol.

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In aquafeeds, fish-meal has been commonly replaced with plant protein, which often causes enteritis. Currently, foodborne enteritis has few solutions in regards to prevention or cures. The recovery mechanism from enteritis in herbivorous fish may further help understand prevention or therapy. However, few reports could be found regarding the recovery or resilience to fish foodborne enteritis. In this study, grass carp was used as an animal model for soybean meal induced enteritis and it was found that the fish could adapt to the soybean meal at a moderate level of substitution. Resilience to soybean meal stress was found in the 40% soybean meal group for juvenile fish at growth performance, morphological and gene expression levels, after a 7-week feeding trial. Furthermore, the intestinal transcriptomic data, including transcriptome and miRNAome, was applied to demonstrate resilience mechanisms. The result of this study revealed that in juvenile grass carp after a 7-week feeding cycle with 40% soybean meal, the intestine recovered via enhancing both an immune tolerance and wound healing, the liver gradually adapted via re-balancing immune responses, such as phagosome and complement cascades. Also, many immune factors in the gut and liver were systemically revealed among stages of on-setting, remising, and recovering (or relief). In addition, miRNA regulation played a key role in switching immune states. Thus, the present data systemically demonstrated that the molecular adaptation mechanism of fish gut-liver immunity is involved in the resilience to soybean meal stress.

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“…Mott et al [19] reported that miR-29b is an important endogenous regulator, which plays a role in endothelial cell apoptosis by inhibiting the anti-apoptotic gene, myeloid cell leukemia-1. Anke and his team also showed that miR-29b mediates the deposition of collagen and fibrosis via IL-6 and tumor growth factor-β [20]. miR-29b has also been suggested to suppress the proliferation and migration of vascular smooth muscle cells, possibly through inhibition of myeloid cell leukemia-1 and matrix metalloproteinase-2, indicating that miR-29b may serve as a valuable therapeutic tool to treat CVD, such as atherosclerosis [21].…”

Section: Discussionmentioning

confidence: 99%

The Association of Circulating MiR-29b and Interleukin-6 with Subclinical Atherosclerosis

Huang

Chen

et al. 2017

Cell Physiol Biochem

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Background/Aims: Although it is widely acknowledged that atherosclerosis is mainly a chronic inflammatory process, in which both miR-29b and interleukin-6 (IL-6) play multifaceted roles, the association between miR-29b and IL-6 remains unknown. The aim of the present study was to explore the relationship between miR-29b and IL-6 and to test whether circulating levels of miR-29b and IL-6 could predict atherosclerosis. Methods: A total of 170 participants were divided into two groups according to carotid intima-media thickness (CIMT): study group (CIMT ≥ 0.9mm) and control group (CIMT < 0.9mm). Levels of circulating miR-29b and IL-6 were measured by quantitative real-time polymerase chain reaction (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA), respectively. The association of miR-29b and IL-6 levels with CIMT was assessed using Spearman correlation analysis and multiple linear regression analysis. Results: The study group showed higher miR-29b levels (31.61 ± 3.05 vs. 27.91 ± 1.71 Ct, p < 0.001) and IL-6 levels (3.40 ± 0.67 vs. 2.99 ± 0.37 pg/ml, p < 0.001), compared with the control group. CIMT was positively correlated with miR-29b (r = 0.587, p < 0.001) and IL-6 (r = 0.410, p < 0.001), and miR-29b levels were also correlated with IL-6 (r = 0.242, p = 0.001). Multiple linear regression analysis also showed that CIMT was positively correlated with miR-29b and IL-6. After adjustment for age, body mass index, systolic blood pressure, total cholesterol and C-reactive protein, CIMT was still closely correlated with miR-29b and IL-6. The combination of miR-29b and IL-6 (AUC = 0.901, p < 0.001) offered a better predictive index for atherosclerosis than either miR-29b (AUC = 0.867, p < 0.001) or IL-6 (AUC = 0.747, p < 0.001) alone. Conclusion: Circulating levels of miR-29b and IL-6 may be independently correlated with subclinical atherosclerosis, and may serve as novel biomarkers for the identification of atherosclerosis.

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MCL-1 is modulated in Crohn’s disease fibrosis by miR-29b via IL-6 and IL-8

Cited by 29 publications

References 47 publications

Intestinal mucosa-derived DNA methylation signatures in the penetrating intestinal mucosal lesions of Crohn’s disease

Intestinal mucosa-derived DNA methylation signatures in the penetrating intestinal mucosal lesions of Crohn’s disease

Integrative Transcriptomic and microRNAomic Profiling Reveals Immune Mechanism for the Resilience to Soybean Meal Stress in Fish Gut and Liver

The Association of Circulating MiR-29b and Interleukin-6 with Subclinical Atherosclerosis

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