Role of miR-195 in cigarette smoke-induced chronic obstructive pulmonary disease

Gu, Wenchao; Yuan, Yaping; Yang, Hua; Wu, Hao; Wang, Linxuan; Tang, Zhijun; Li, Qiang

doi:10.1016/j.intimp.2017.11.030

Cited by 28 publications

(20 citation statements)

References 25 publications

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“…Anti-miR-195 increased the protein level of PHLPP2, and decreased p-AKT in the lungs of CS-exposed mice. Altogether, miR-195 targeted PHLPP2 and also promoted the release of IL-6 and TNF-α, an observation similar to knockdown of PHLPP2 in BEAS-2B cells [55].…”

Section: Copdmentioning

confidence: 56%

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miRNAs in Lung Development and Diseases

Boateng

Krauss‐Etschmann

2020

IJMS

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The development of the lung involves a diverse group of molecules that regulate cellular processes, organ formation, and maturation. The various stages of lung development are marked by accumulation of small RNAs that promote or repress underlying mechanisms, depending on the physiological environment in utero and postnatally. To some extent, the pathogenesis of various lung diseases is regulated by small RNAs. In this review, we discussed miRNAs regulation of lung development and diseases, that is, COPD, asthma, pulmonary fibrosis, and pulmonary arterial hypertension, and also highlighted possible connotations for human lung health.After fertilization in the mouse, total miRNA in the two-cell-stage embryo was demonstrated to be significantly lower than the levels in one-cell zygote [15]. Notably, total miRNA in the four-cell-stage embryo was higher than the levels in the two-cell-stage embryo [15]. In the early mouse embryo, miR-127 was upregulated at E6.5 and E7.5 [16]. Overexpression of miR-127 in mouse embryonic stem cells, which differentiated into embryoid bodies, increased the mRNA levels of Gsc, Foxa2, and Brachyury (mesendoderm markers), but elicited no change in Pax6 and Otx2 (ectoderm markers) three days after transfection. Inhibition of miR-127 showed opposite regulation of Gsc, Foxa2, and Brachyury. miR-127, moreover, was suggested to control mesendoderm differentiation [16]. miR-326 regulated sonic hedgehog signaling by targeting Smo and Gli2 [17]. The inhibition of smoothened in cultured explanted E12 mouse lung resulted in the expansion of distal epithelium, and disruption of normal branching pattern and mesenchymal integrity [17]. Another study described the functional role of miR-142-3p in the mouse embryonic lung mesenchyme. The miRNA was shown to regulate adenomatous polyposis coli to further modulate Wnt signaling [18]. Taken together, miR-142-3p regulated the proliferation and differentiation of mesenchymal progenitors in the mouse embryonic lung [18].In the developing mouse lung, the level of miR-17 was stable (E11.5-E16.5), predominantly at the pseudoglandular stage, with higher epithelial levels at E12.5 [19]. Simultaneous knockdown of miR-17 and its paralogs, miR-20a and miR-106b, for 72 h in epithelial lung explants altered branching, even in FGF10-treated condition [19]. In the human fetal lung, miR-449a was upregulated at 18-20 weeks (canalicular stage), and in the mouse embryonic lung, miR-449a level was increased from E15.5 to E18.5 [20]. The inhibition of miR-449a in E16.5 mouse lung culture (end of pseudoglandular stage) increased the mRNA levels of Mycn and Sox9, and the protein levels of Ki-67 and SOX9 particularly in the distal epithelial region [20].Knockout of miR-26a-1/miR-26a-2 in the mouse promoted the formation of dilated lumens and aerated regions at the beginning of the canalicular stage (E16.5) of lung development [21]. Results at the saccular stage (E18.5) also indicated large lamellar bodies, and increased SP-A, SP-B, and SP-C protein levels in miR-26a knockout mice....

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Section: Copdmentioning

confidence: 56%

“…The inhibition of miR-130a in CSE-treated BEAS-2B cells upregulated the protein levels of WNT1, β-catenin, and LEF1 [54]. In an earlier study, intranasal administration of anti-miR-195 to mice mitigated CS-induced disruption of the lungs [55]. Anti-miR-195 increased the protein level of PHLPP2, and decreased p-AKT in the lungs of CS-exposed mice.…”

Section: Copdmentioning

confidence: 81%

miRNAs in Lung Development and Diseases

Boateng

Krauss‐Etschmann

2020

IJMS

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“…MiR - 195 was highly expressed in peripheral lung tissues from COPD patients compared to the levels found in never smokers. Knocking down miR - 195 alleviates CS-induced lung injury and inflammatory cell infiltration, as well as production of TNF - α and IL - 6 , by regulating Akt signaling [176], indicating that miR - 195 has a role in the promotion of inflammation. However, there are still disputes about the effects of miR-195 on inflammation.…”

Section: Epigenetics and Inflammationmentioning

confidence: 99%

The role of cigarette smoke-induced epigenetic alterations in inflammation

Zong

Liu

et al. 2019

Epigenetics & Chromatin

130

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Background: Exposure to cigarette smoke (CS) is a major threat to human health worldwide. It is well established that smoking increases the risk of respiratory diseases, cardiovascular diseases and different forms of cancer, including lung, liver, and colon. CS-triggered inflammation is considered to play a central role in various pathologies by a mechanism that stimulates the release of pro-inflammatory cytokines. During this process, epigenetic alterations are known to play important roles in the specificity and duration of gene transcription. Main text: Epigenetic alterations include three major modifications: DNA modifications via methylation; various posttranslational modifications of histones, namely, methylation, acetylation, phosphorylation, and ubiquitination; and non-coding RNA sequences. These modifications work in concert to regulate gene transcription in a heritable fashion. The enzymes that regulate these epigenetic modifications can be activated by smoking, which further mediates the expression of multiple inflammatory genes. In this review, we summarize the current knowledge on the epigenetic alterations triggered by CS and assess how such alterations may affect smoking-mediated inflammatory responses. Conclusion: The recognition of the molecular mechanisms of the epigenetic changes in abnormal inflammation is expected to contribute to the understanding of the pathophysiology of CS-related diseases such that novel epigenetic therapies may be identified in the near future.

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“…miRNA has been confirmed to be related to COPD and smoking. It plays an important role in the development of COPD [78,79]. Conickx et al [80] exposed mice to air and CS for twenty-four weeks and detected differential expression profiles of miRNAs in mice lung tissue and bronchoalveolar lavage fluid.…”

Section: Mirna and Pulmonary Vascular Endothelial Cell Apoptosismentioning

confidence: 99%

The role of cigarette smoke-induced pulmonary vascular endothelial cell apoptosis in COPD

2021

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Chronic obstructive pulmonary disease (COPD) is one of the most common chronic respiratory diseases with high morbidity and mortality. It has become the fifth most burdened and the third most deadly disease in the global economy and increases year by year. The prevention and treatment of COPD are urgent. Smoking is the main and most common risk factor for COPD. Cigarette smoke (CS) contains a large number of toxic substances, can cause a series of changes in the trachea, lung tissue, pulmonary blood vessels, and promotes the occurrence and development of COPD. In recent years, the development of epigenetics and molecular biology have provided new guidance for revealing the pathogenesis, diagnosis, and treatment of diseases. The latest research indicates that pulmonary vascular endothelial cell apoptosis initiates and participates in the pathogenesis of COPD. In this review, we summarize the current research on the epigenetic mechanisms and molecular biology of CS-induced pulmonary vascular endothelial cell apoptosis in COPD, providing a new research direction for pathogenesis of COPD and a new target for the diagnosis, treatment, and prevention of COPD.

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Role of miR-195 in cigarette smoke-induced chronic obstructive pulmonary disease

Cited by 28 publications

References 25 publications

miRNAs in Lung Development and Diseases

miRNAs in Lung Development and Diseases

The role of cigarette smoke-induced epigenetic alterations in inflammation

The role of cigarette smoke-induced pulmonary vascular endothelial cell apoptosis in COPD

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