Downregulation of miR-133 and miR-590 contributes to nicotine-induced atrial remodelling in canines

Shan, Hongli; Zhang, Yong; Lu, Yanjie; Zhang, Ying; Pan, Zhenwei; Cai, Benzhi; Wang, Ning; Li, Xuelian; Feng, Tingting; Hong, Yuan; Yang, Baofeng

doi:10.1093/cvr/cvp130

Cited by 315 publications

(252 citation statements)

References 55 publications

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“…In addition, we have observed that the ␣7 nAChR blockade enhances the expression of transglutaminase, a marker of squamous differentiation known to be up-regulated by TGF-␤. 38 Moreover, upregulation of TGF-␤ by nicotine is mediated by ␣7 nAChR during atrial remodeling, 65 TGF-␤ up-regulates CK14 expression and promotes the expression of basal cell phenotype 66 and inhibits p63 function. 67 Taken together, our results suggest that ␣7 nAChRs inactivation can initiate an alternative program of the basal cell differentiation process leading to squamous differentiation and that this process may be associated to down-regulation of Foxj1 and/or up-regulation of TGF-␤.…”

Section: Discussionmentioning

confidence: 99%

α7 Nicotinic Acetylcholine Receptor Regulates Airway Epithelium Differentiation by Controlling Basal Cell Proliferation

Maouche

Polette

Jolly

et al. 2009

The American Journal of Pathology

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Airway epithelial basal cells are known to be critical for regenerating injured epithelium and maintaining tissue homeostasis. Recent evidence suggests that the ␣7 nicotinic acetylcholine receptor (nAChR), which is highly permeable to Ca 2؉ , is involved in lung morphogenesis. Here, we have investigated the potential role of the ␣7 nAChR in the regulation of airway epithelial basal cell proliferation and the differentiation of the human airway epithelium. In vivo during fetal development and in vitro during the regeneration of the human airway epithelium, ␣7 nAChR expression coincides with epithelium differentiation. Inactivating ␣7 nAChR function in vitro increases cell proliferation during the initial steps of the epithelium regeneration, leading to epithelial alterations such as basal cell hyperplasia and squamous metaplasia, remodeling observed in many bronchopulmonary diseases. The regeneration of the airway epithelium after injury in ␣7 The respiratory epithelium, which is constantly exposed to airborne pollutants, is frequently injured, which results in altered epithelial functions. To restore these functions, the respiratory epithelium must undergo rapid repair via epithelial cell spreading and migration and regenerate its structure via basal cell proliferation and differentiation.

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Section: Discussionmentioning

confidence: 99%

α7 Nicotinic Acetylcholine Receptor Regulates Airway Epithelium Differentiation by Controlling Basal Cell Proliferation

Maouche

Polette

Jolly

et al. 2009

The American Journal of Pathology

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“…For example, miR‐133 and miR‐590 are both down‐regulated in a canine model of nicotine‐induced AF, leading to increased expression of TGF‐β1 and TGFβRII 43. Expression of miR‐29 was decreased in the left atrium of dogs with heart failure, which develop an AF‐maintaining fibrotic substrate 7, 44.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‐30c suppresses the pro‐fibrogenic effects of cardiac fibroblasts induced by TGF‐β1 and prevents atrial fibrosis by targeting TGFβRII

Wang

Chen

et al. 2018

J Cellular Molecular Medi

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Atrial fibrosis serves as an important contributor to atrial fibrillation (AF). Recent data have suggested that microRNA‐30c (miR‐30c) is involved in fibrotic remodelling and cancer development, but the specific role of miR‐30c in atrial fibrosis remains unclear. The purpose of this study was to investigate the role of miR‐30c in atrial fibrosis and its underlying mechanisms through in vivo and in vitro experiments. Our results indicate that miR‐30c is significantly down‐regulated in the rat abdominal aortic constriction (AAC) model and in the cellular model of fibrosis induced by transforming growth factor‐β1 (TGF‐β1). Overexpression of miR‐30c in cardiac fibroblasts (CFs) markedly inhibits CF proliferation, differentiation, migration and collagen production, whereas decrease in miR‐30c leads to the opposite results. Moreover, we identified TGFβRII as a target of miR‐30c. Finally, transferring adeno‐associated virus 9 (AAV9)‐miR‐30c into the inferior vena cava of rats attenuated fibrosis in the left atrium following AAC. These data indicate that miR‐30c attenuates atrial fibrosis via inhibition of CF proliferation, differentiation, migration and collagen production by targeting TGFβRII, suggesting that miR‐30c might be a novel potential therapeutic target for preventing atrial fibrosis.

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“…miR-133 and miR-328 were selected as likely interactors. Of the two selected miRNAs, miR-133 has been previously described as a muscle-specific miRNA, which has been investigated primarily with regard to the heart (21,22). Therefore, miR-328, a known tumor suppressor, was selected for further analysis.…”

Section: As 2 O 3 Upregulates Expression Of Mir-328 and Downregulatesmentioning

confidence: 99%

Arsenic trioxide inhibits breast cancer cell growth via microRNA-328/hERG pathway in MCF-7 cells

Wang

Yin

et al. 2012

Molecular Medicine Reports

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Abstract. Arsenic trioxide (As 2 O 3 ) has been widely used in the treatment of acute promyelocytic leukemia and has been observed to exhibit therapeutic effects in various types of solid tumor. In a previous study by this group, it was shown that As 2 O 3 induces the apoptosis of MCF-7 breast cancer cells through inhibition of the human ether-à-go-go-related gene (hERG) channel. The present study was designed to further investigate the effect of As 2 O 3 on breast cancer cells and to examine the mechanism underlying the regulation of hERG expression. The present study confirmed that As 2 O 3 inhibited tumor growth in vivo, following MCF-7 cell implantation into nude mice. Using computational prediction , it was identified that microRNA (miR)-328 had a binding site in the 3'-untranslated region of hERG mRNA. A luciferase activity assay demonstrated that hERG is a target gene of miR-328. Further investigation using western blot analysis and reverse transcription-quantitative polymerase chain reaction revealed that As 2 O 3 downregulated hERG expression via upregulation of miR-328 expression in MCF-7 cells. In conclusion, As 2 O 3 was observed to inhibit breast cancer cell growth, at least in part, through the miR-328/hERG pathway.

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Downregulation of miR-133 and miR-590 contributes to nicotine-induced atrial remodelling in canines

Abstract: We conclude that the profibrotic response to nicotine in canine atrium is critically dependent upon downregulation of miR-133 and miR-590.

Cited by 315 publications

References 55 publications

α7 Nicotinic Acetylcholine Receptor Regulates Airway Epithelium Differentiation by Controlling Basal Cell Proliferation

α7 Nicotinic Acetylcholine Receptor Regulates Airway Epithelium Differentiation by Controlling Basal Cell Proliferation

MicroRNA‐30c suppresses the pro‐fibrogenic effects of cardiac fibroblasts induced by TGF‐β1 and prevents atrial fibrosis by targeting TGFβRII

Arsenic trioxide inhibits breast cancer cell growth via microRNA-328/hERG pathway in MCF-7 cells

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