Regulation of Smooth Muscle Contractility by Competing Endogenous mRNAs in Intracranial Aneurysms

Zhang, Mingming; Ren, Yuan; Wang, Yajie; Wang, Renzhi; Zhou, Qian; Peng, Yong; Li, Qi; Yu, Meihong; Jiang, Yugang

doi:10.1097/nen.0000000000000185

Cited by 14 publications

(13 citation statements)

References 41 publications

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“…This indicates there will be ongoing revision of the human genome as previously annotated lncRNAs emerge as mRNAs. Whether encoding a peptide or not, it seems that a noncoding function of any transcript can no longer be ignored [215, 229]. Finally, it will be important to determine whether any relevant SNPs exist in a putative lncRNA using LincSNP (http://210.46.85.180:8080/LincSNP/search.jsp) [230] or lncRNASNP (http://bioinfo.life.hust.edu.cn/lncRNASNP/) [231].…”

Section: Discussionmentioning

confidence: 99%

The short and long of noncoding sequences in the control of vascular cell phenotypes

Miano

Long

2015

Cell. Mol. Life Sci.

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The two principal cell types of importance for normal vessel wall physiology are smooth muscle cells and endothelial cells. Much progress has been made over the past 20 years in the discovery and function of transcription factors that coordinate proper differentiation of these cells and the maintenance of vascular homeostasis. More recently, the converging fields of bioinformatics, genomics, and next generation sequencing have accelerated discoveries in a number of classes of noncoding sequences, including transcription factor binding sites (TFBS), microRNA genes, and long noncoding RNA genes, each of which mediates vascular cell differentiation through a variety of mechanisms. Alterations in the nucleotide sequence of key TFBS or deviations in transcription of noncoding RNA genes likely have adverse effects on normal vascular cell phenotype and function. Here, the subject of noncoding sequences that influence smooth muscle cell or endothelial cell phenotype will be summarized as will future directions to further advance our understanding of the increasingly complex molecular circuitry governing normal vascular cell differentiation and how such information might be harnessed to combat vascular diseases.

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Section: Discussionmentioning

confidence: 99%

The short and long of noncoding sequences in the control of vascular cell phenotypes

Miano

Long

2015

Cell. Mol. Life Sci.

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“…Only two studies were performed in dogs. Almost half of the mouse models were employed in transgenic animals [22,41,43,53,92,95,96,99,102,105,106,109,112,114,127].…”

Section: Resultsmentioning

confidence: 99%

Preclinical Intracranial Aneurysm Models: A Systematic Review

et al. 2020

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Intracranial aneurysms (IA) are characterized by weakened cerebral vessel walls that may lead to rupture and subarachnoid hemorrhage. The mechanisms behind their formation and progression are yet unclear and warrant preclinical studies. This systematic review aims to provide a comprehensive, systematic overview of available animal models for the study of IA pathobiology. We conducted a systematic literature search using the PubMed database to identify preclinical studies employing IA animal models. Suitable articles were selected based on predefined eligibility criteria following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. Included studies were reviewed and categorized according to the experimental animal and aneurysm model. Of 4266 returned results, 3930 articles were excluded based on the title and/or abstract and further articles after screening the full text, leaving 123 studies for detailed analysis. A total of 20 different models were found in rats (nine), mice (five), rabbits (four), and dogs (two). Rat models constituted the most frequently employed intracranial experimental aneurysm model (79 studies), followed by mice (31 studies), rabbits (12 studies), and two studies in dogs. The most common techniques to induce cerebral aneurysms were surgical ligation of the common carotid artery with subsequent induction of hypertension by ligation of the renal arteries, followed by elastase-induced creation of IAs in combination with corticosterone- or angiotensin-induced hypertension. This review provides a comprehensive summary of the multitude of available IA models to study various aspects of aneurysm formation, growth, and rupture. It will serve as a useful reference for researchers by facilitating the selection of the most appropriate model and technique to answer their scientific question.

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“…We chose MYOCD and miR-9 as a model system because: 1) miR-9 was reported to be differentially expressed in IA SMCs in comparison to the normal control [27]; 2) it has been confirmed that MYOCD is essential in the process of enhancing contractility of vessels by expressing a unique group of signaling molecules, contractile agonist receptors, and contractile proteins to fulfill the task [28,29]; 3) delicate expression level change of MYOCD was critical in determining percentage of survival and IA was demonstrated by the IA mouse model [30]; and 4) partial or complete loss of MYOCD can lead to dramatic deceleration of IA in the IA mouse model [13]. …”

Section: Discussionmentioning

confidence: 99%

“…SMC contractile assay was used to determine the contractility of SMCs with different treatments, as previously described [13]. …”

Section: Methodsmentioning

confidence: 99%

“…Zhang et al identified many miRNAs that were differentially expressed in the smooth muscle cells collected from the patients with IA compared to those without IA; miR-9 is one of those differentially expressed miRNAs [13]. Using the online miRNA database, we found that MYOCD is a virtual target of miR-9, and MYOCD has been reported to be involved in the pathogenesis of IA by regulating the contractility of smooth muscle cells [14].…”

Section: Introductionmentioning

confidence: 99%

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Aberrant Expression of microRNA-9 Contributes to Development of Intracranial Aneurysm by Suppressing Proliferation and Reducing Contractility of Smooth Muscle Cells

et al. 2016

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BackgroundMiR-9 is reportedly involved with many diseases, such as acute myeloid leukemia and liver oncogenesis. In the present study we investigated the molecular mechanism, including the potential regulator and signaling pathways, of MYOCD, which is the gene that in humans encodes the protein myocardin.Material/MethodsWe searched the online miRNA database (www.mirdb.org) with the “seed sequence” located within the 3′-UTR of the target gene, and then validated MYOCD to be the direct gene via luciferase reporter assay system, and further confirmed it in cultured cells by using Western blot analysis and realtime PCR.ResultsWe established the negative regulatory relationship between miR-9 and MYOCD via studying the relative luciferase activity. We also conducted realtime PCR and Western blot analysis to study the mRNA and protein expression level of MYOCD between different groups (intracranial aneurysm vs. normal control) or cells treated with scramble control, miR-9 mimics, MYOCD siRNA, and miR-9 inhibitors, indicating the negative regulatory relationship between miR-9 and MYOCD. We also investigated the relative viability of smooth muscle cells when transfected with scramble control, miR-9 mimics, MYOCD siRNA, and miR-9 inhibitors to validate that miR-9 t negatively interferes with the viability of smooth muscle cells. We then investigated the relative contractility of smooth muscle cells when transfected with scramble control, miR-9 mimics, MYOCD siRNA, and miR-9 inhibitors, and the results showed that miR-9 weakened contractility.ConclusionsOur findings show that dysregulation of miR-9 is responsible for the development of IA via targeting MYOCD. miR-9 and its direct target, MYOCD, might novel therapeutic targets in the treatment of IA.

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Regulation of Smooth Muscle Contractility by Competing Endogenous mRNAs in Intracranial Aneurysms

Cited by 14 publications

References 41 publications

The short and long of noncoding sequences in the control of vascular cell phenotypes

The short and long of noncoding sequences in the control of vascular cell phenotypes

Preclinical Intracranial Aneurysm Models: A Systematic Review

Aberrant Expression of microRNA-9 Contributes to Development of Intracranial Aneurysm by Suppressing Proliferation and Reducing Contractility of Smooth Muscle Cells

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