Roles of microRNAs in atherosclerosis and restenosis

Chen, Li Jing; Lim, Seh Hong; Yeh, Yi Ting; Lien, Sheng Chieh; Chiu, Jeng Jiann

doi:10.1186/1423-0127-19-79

Cited by 70 publications

(95 citation statements)

References 103 publications

(117 reference statements)

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“…To examine the cell migratory capacity, 1x10 5 cells/well MCF-7 cells in each group were cultured in DMEM with 10% FBS to 100% confluence. Wounds of ~1 mm width were created with a plastic scriber and cells were washed once using PBS.…”

Section: Methodsmentioning

confidence: 99%

“…By negatively mediating their target genes, miRs participate in a variety of cellular biological processes including cell growth and proliferation, survival and apoptosis, differentiation, migration and invasion (5)(6)(7)(8). Furthermore, it has been demonstrated that the deregulation of certain miRs, such as miR-375, are involved in tumorigenesis and tumor metastasis (9-11).…”

Section: Introductionmentioning

confidence: 99%

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MicroRNA-375 targets PAX6 and inhibits the viability, migration and invasion of human breast cancer MCF-7 cells

Zou

Huang

et al. 2017

Experimental and Therapeutic Medicine

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Abstract. MicroRNAs (miRs) are a type of small non-coding RNA that serve crucial roles in the development and progression of breast cancer. However, the exact role and underlying molecular mechanism of miR-375 in mediating the growth and metastasis of breast cancer remains unknown. In the present study, reverse transcription-quantitative polymerase chain reaction and western blot analysis were conducted to examine RNA and protein expression. A luciferase reporter assay was performed to determine the association between miR-375 and paired box 6 (PAX6). The results of the current study indicate that the expression of miR-375 was reduced in breast cancer tissues compared with matched adjacent normal tissues. Transfection with miR-375 mimics led to a significant increase in levels of miR-375 in human breast cancer Michigan Cancer Foundation (MCF)-7 cells (P<0.05). The increase in miR-375 expression caused a significant decrease in the viability, migration and invasion of MCF-7 cells (P<0.05), accompanied by a reduced expression of matrix metalloproteinase (MMP) 2 and MMP9 proteins. Luciferase reporter assay identified PAX6 as a novel target of miR-375 and miR-375 in turn, negatively regulated the protein expression of PAX6 in MCF-7 cells. By contrast, overexpression of PAX6 led to a significant increase in MCF-7 cell viability (P<0.01) but did not affect the migration and invasion of MCF-7 cells, suggesting that the inhibitory effect of miR-375 on MCF-7 cell viability may be occurring, in part, via the direct targeting of PAX6.

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Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

MicroRNA-375 targets PAX6 and inhibits the viability, migration and invasion of human breast cancer MCF-7 cells

Zou

Huang

et al. 2017

Experimental and Therapeutic Medicine

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“…It has been reported that miRNAs are highly conserved among species and are crucial in various physiological and pathological processes, including age-associated diseases, developmental abnormalities, autoimmune diseases and various types of cancer (18)(19)(20)(21). The role of miRNAs in the cardiovascular system has been previously investigated (22,23); however, the function of miRNAs in the proliferation of VSMCs induced by TNF-α remains to be fully investigated.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of microRNA-25 by tumor necrosis factor α is critical in the modulation of vascular smooth muscle cell proliferation

Zhi

Zhang

et al. 2015

Molecular Medicine Reports

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Abstract. Atherosclerosis and coronary heart disease are characterized by a hyperplastic neointima and inflammation involving cytokines, such as tumor necrosis factor-α (TNF-α). TNF-α is pleiotropic and mediates inflammation and proliferation in various cell types, such as vascular smooth muscle cells (VSMCs). The molecular mechanism for the pleiotropic effects of TNF-α has not previously been fully elucidated. The current study identified that the expression of microRNA-25 (miR-25), a small noncoding RNA, was reduced in response to TNF-α signaling in VSMCs. Restored miR-25 expression inhibited cell proliferation and Ki-67 expression. The present study indicated that cyclin-dependent kinase 6 (CDK6) was the direct target gene of miR-25 using mRNA and protein expression analysis, and luciferase assays. It was also observed that restored CDK6 expression in the miR-25 mimic-treated VSMCs partly reduced miR-25-mediated VSMC proliferation. In conclusion, miR-25 is suggested to be important in TNF-α-induced abnormal proliferation of VSMCs.

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“…It has been revealed that miRNAs regulate >30% of genes, which are associated with almost all major cellular processes, including cell proliferation, differentiation, apoptosis and migration, as well as immune responses (4). Myocardial tissue injury induced by ischemia and hypoxia is a major factor underlying the development of fatal diseases.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of microRNA-101 attenuates hypoxia/reoxygenation-induced apoptosis through induction of autophagy in H9c2 cardiomyocytes

Jiang

Chen

et al. 2015

Molecular Medicine Reports

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Abstract. Autophagy is a cellular self-catabolic process responsible for the degradation of proteins and organelles. Autophagy is able to promote cell survival in response to stress, and increased autophagy amongst cardiomyocytes has been identified in conditions of heart failure, starvation and ischemia/reperfusion. However, the detailed regulatory mechanisms underlying autophagy in heart disease have remained elusive. MicroRNAs (miRNAs) have been implicated in the regulation of autophagy in cells under stress. In the present study, the protective effect of miRNA (miR)-101 on hypoxia/reoxygenation (H/R)-induced cardiomyocyte apoptosis was investigated. It was revealed that H/R induced apoptosis in H9c2 cardiomyocytes, accompanied by a downregulation of miR-101 expression. Further investigation identified Ras-related protein Rab-5A (RAB5A) as a direct target of miR-101. RAB5A was previously reported to be involved in autophagy; therefore, the present study further focused on the role of miR-101 in the regulation of autophagy under H/R and found that the inhibition of miR-101 attenuated H/R-induced apoptosis, at least partially, via the induction of autophagy. In conclusion, the results of the present study revealed a beneficial effect of miR-101 inhibition on H/R-induced apoptosis in cardiomyocytes, indicating that miR-101 inhibition may present a potential therapeutic agent in the treatment or prevention of heart diseases. IntroductionAutophagy is a cellular self-catabolic process responsible for the degradation of long-lived proteins and organelles. During autophagy, cytoplasmic constituents are sequestered into autophagosomes and degraded via the lysosomal pathway (1).Autophagy is able to promote cell survival in response to stress. However, progressive autophagy also induces cell death (2). Therefore, autophagy not only has a crucial role in the regulation of normal development, but dysregulated or defective autophagy is associated with disease.MicroRNAs (miRNAs) are a group of endogenous, non-coding, single-strand, small RNAs of 22-25 nucleotides, which regulate gene expression at the post-transcriptional level, predominantly through base pairing with the 3'-untranslated region (3'-UTR) of target mRNAs, which results in mRNA degradation or translational repression (3). It has been revealed that miRNAs regulate >30% of genes, which are associated with almost all major cellular processes, including cell proliferation, differentiation, apoptosis and migration, as well as immune responses (4). Myocardial tissue injury induced by ischemia and hypoxia is a major factor underlying the development of fatal diseases. The main cause of myocardial ischemic injury is myocardial cell apoptosis induced by myocardial hypoxia (5). Furthermore, subsequent reoxygenation may further aggravate the damage (6). Multiple miRNAs have been shown to function as protectors against hypoxia/reoxygenation (H/R)-induced myocardial injury (7-9). However, the specific molecular mechanisms underlying this effect have remained elusive.Accumu...

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Roles of microRNAs in atherosclerosis and restenosis

Cited by 70 publications

References 103 publications

MicroRNA-375 targets PAX6 and inhibits the viability, migration and invasion of human breast cancer MCF-7 cells

MicroRNA-375 targets PAX6 and inhibits the viability, migration and invasion of human breast cancer MCF-7 cells

Inhibition of microRNA-25 by tumor necrosis factor α is critical in the modulation of vascular smooth muscle cell proliferation

Inhibition of microRNA-101 attenuates hypoxia/reoxygenation-induced apoptosis through induction of autophagy in H9c2 cardiomyocytes

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