Expression of apoptosis-associated microRNAs in ethanol-induced acute gastric mucosal injury via JNK pathway

Luo, Xiu-Ju; Liu, Bin; Dai, Zhong; Li, Ting-Bo; Li, Nian-Sheng; Zhang, Xiaojie; Yang, Zhi-Chun; Li, Yuan‐Jian; Peng, Jun

doi:10.1016/j.alcohol.2013.05.005

Cited by 37 publications

(27 citation statements)

References 46 publications

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“…, demonstrate that miR‐145 expression is inhibited through activation of the MAPK and JNK pathways in colorectal cancer. Furthermore, in cardiomyocytes, the protective activity of miR‐145 is associated with modulation of both MEK‐1/2 and JNK and in gastric mucosal epithelial cell regulation of miR‐145 involves JNK . Similar to our results, p38 has previously been shown to be linked to miR‐145 induction in VSMCs and Hong et al .…”

Section: Discussionsupporting

confidence: 91%

Airway smooth muscle inflammation is regulated by microRNA‐145 in COPD

et al. 2016

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Chronic obstructive pulmonary disease (COPD) is a common, highly debilitating disease of the airways, primarily caused by smoking. Chronic inflammation and structural remodelling are key pathological features of this disease, in part caused by the aberrant function of airway smooth muscle (ASM) cells under the regulation of transforming growth factor (TGF)‐β. miRNA are short, noncoding gene transcripts involved in the negative regulation of specific target genes, through their interactions with mRNA. Previous studies have proposed that mRNA‐145 (miR‐145) may interact with SMAD3, an important downstream signalling molecule of the TGF‐β pathway. TGF‐β was used to stimulate primary human ASM cells isolated from healthy nonsmokers, healthy smokers and COPD patients. This resulted in a TGF‐β‐dependent increase in CXCL8 and IL‐6 release, most notably in the cells from COPD patients. TGF‐β stimulation increased SMAD3 expression, only in cells from COPD patients, with a concurrent increased miR‐145 expression. Regulation of miR‐145 was found to be negatively controlled by pathways involving the MAP kinases, MEK‐1/2 and p38 MAPK. Subsequent, overexpression of miR‐145 (using synthetic mimics) in ASM cells from patients with COPD suppressed IL‐6 and CXCL8 release, to levels comparable to the nonsmoker controls. Therefore, this study suggests that miR‐145 negatively regulates pro‐inflammatory cytokine release from ASM cells in COPD by targeting SMAD3.

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Section: Discussionsupporting

confidence: 91%

Airway smooth muscle inflammation is regulated by microRNA‐145 in COPD

et al. 2016

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“…JNK signaling mediates EPH receptor A2-dependent tumor cell proliferation, motility and cancer stem cell-like properties in NSCLC cells (36). miR-145 induces apoptosis in ethanol-induced acute gastric mucosal injury via the JNK signaling pathway (37). However, no studies have yet shown the association between miR-145-5p and the JNK signaling pathway in NSCLC.…”

Section: Discussionmentioning

confidence: 99%

miR‑145‑5p inhibits epithelial‑mesenchymal transition via the JNK signaling pathway by targeting MAP3K1 in non‑small cell lung cancer cells

et al. 2017

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Abstract. Lung cancer is one of the most common types of tumors and the leading cause of cancer-associated mortality in the world. Additionally, non-small cell lung cancer (NSCLC) accounts for ~80% of all lung cancer cases. Epithelialmesenchymal transition (EMT) is an important cell biological process, which is associated with cancer migration, metastasis, asthma and fibrosis in the lung. In the present study, it was revealed that miR-145-5p was able to suppress EMT by inactivating the c-Jun N-terminal kinase (JNK) signaling pathway in NSCLC cells. Mitogen-activated protein kinase kinase kinase 1 (MAP3K1) was predicted and confirmed to be a novel target of miR-145-5p. Overexpression of MAP3K1 was able to reverse the inhibition of EMT induced by miR-145-5p via the JNK signaling pathway. Overall, the results revealed that miR-145-5p inhibits EMT via the JNK signaling pathway by targeting MAP3K1 in NSCLC cells.

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“…1D) regardless the inhibition of Wnt signaling mediated by chronic ethanol exposure. It is not unexpected since it has been reported that chronic ethanol treatment increased c-Jun mRNA expression (Park et al, 2012) and acute ethanol-induced apoptosis was mediated via c-Jun N-terminal kinase (JNK) pathway with enhanced JNK activity (Luo et al, 2013). Thus, Jun expression may be affected by other signaling rather than Wnt pathway in this experimental condition.…”

Section: Discussionmentioning

confidence: 99%

Chronic Ethanol‐Induced Impairment of Wnt/β‐Catenin Signaling is Attenuated by PPAR‐δ Agonist

Tong

Huang

et al. 2015

Alcoholism Clin & Exp Res

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Background The Wnt/β-catenin pathway regulates liver growth, repair, and regeneration. Chronic ethanol exposure blunts normal liver regenerative responses, in part by inhibiting insulin/IGF signaling, and correspondingly, previous studies showed that ethanol-impaired liver regeneration could be restored by insulin sensitizer (PPAR-δ agonist) treatment. Since Wnt/β-catenin functions overlap and crosstalk with insulin/IGF pathways, we investigated the effects of ethanol exposure and PPAR-δ agonist treatment on Wnt pathway gene expression in relation to liver regeneration. Methods Adult male Long Evans rats were fed with isocaloric liquid diets containing 0% or 37% ethanol for 8 weeks, and also treated with vehicle or a PPAR-δ agonist during the last 3 weeks of the feeding regimen. The rats were then subjected to 70% partial hepatectomy (PH) and livers harvested at various post-PH time points were used to quantify expression of 19 Wnt pathway genes using Quantigene 2.0 Multiplex Assay. Results Ethanol broadly inhibited expression of Wnt/β-catenin signaling-related genes, including down-regulation of Wnt1, Fzd3, Lef1, and Bcl9 throughout the post-PH time course (0-72 h), and suppression of Wnt7a, Ccnd1, Fgf4, Wif1, Sfrp2, and Sfrp5 at 18, 24 hours post-PH time points. PPAR-δ agonist treatments rescued the ethanol-induced suppression of Wnt1, Wnt7a, Fzd3, Lef1, Bcl9, Ccnd1, and Sfrp2 gene expression in liver, corresponding with the improvements in DNA synthesis and restoration of hepatic architecture. Conclusions Chronic high-dose ethanol exposures inhibit Wnt signaling, which likely contributes to the impairments in liver regeneration. Therapeutic effects of PPAR-δ agonists extend beyond restoration of insulin/IGF signaling mechanisms and are mediated in part by enhancement of Wnt pathway signaling. Future studies will determine the degree to which targeted restoration of Wnt signaling is sufficient to improve liver regeneration and remodeling in the context of chronic ethanol exposure.

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Expression of apoptosis-associated microRNAs in ethanol-induced acute gastric mucosal injury via JNK pathway

Cited by 37 publications

References 46 publications

Airway smooth muscle inflammation is regulated by microRNA‐145 in COPD

Airway smooth muscle inflammation is regulated by microRNA‐145 in COPD

miR‑145‑5p inhibits epithelial‑mesenchymal transition via the JNK signaling pathway by targeting MAP3K1 in non‑small cell lung cancer cells

Chronic Ethanol‐Induced Impairment of Wnt/β‐Catenin Signaling is Attenuated by PPAR‐δ Agonist

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