Microarray profiling of long non-coding RNA (lncRNA) associated with hypertrophic cardiomyopathy

Yang, Wei; Li, Yuan; He, Fuqiang; Wu, Hao

doi:10.1186/s12872-015-0056-7

Cited by 52 publications

(49 citation statements)

References 35 publications

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“…After washing and staining the slides, the arrays were scanned using the Agilent Scanner G2505C (Agilent Technologies). The scanned images were analyzed using the Feature Extraction software (version10.7.1.1, Agilent Technologies) and GeneSpring software (version 12.5; Agilent Technologies) [25]. …”

Section: Methodsmentioning

confidence: 99%

Long Non-Coding RNA: Potential Diagnostic and Therapeutic Biomarker for Major Depressive Disorder

Cui

Sun²,

Niu

et al. 2016

Med Sci Monit

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BackgroundThe criteria for diagnosing depression are based on behavioral observation and self-reporting of symptoms by the patients or guardians without any biological validation of the disease. This study aimed to identify long non-coding RNAs (lncRNAs) in peripheral blood mononuclear cells (PBMCs) as robust and predictive biomarkers for diagnosis and therapy response in major depressive disorder (MDD).Material/MethodsWe used human lncRNA 3.0 microarray profiling (which covers 30,586 human lncRNAs), using PBMCs from five MDD patients and five controls. Differentially expressed lncRNAs in the PBMCs of MDD patients were identified, of which 10 candidate lncRNAs were selected for real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR) analysis in a larger cohort of 138 MDD patients and 63 healthy controls. Then among the 138 MDD patients who received standard antidepressant treatment, 30 were randomly selected for lncRNAs expression retesting and symptomatology assessments after three-weeks and six-weeks of antidepressant treatment.ResultsSix lncRNAs (TCONS_00019174, ENST00000566208, NONHSAG045500, ENST00000517573, NONHSAT034045, and NONHSAT142707) were significantly downregulated in MDD patients compared to control patients, and the area under the receiver operator curve (ROC) of these six lncRNAs cases, combined, was 0.719 (95% confidence interval (CI): 0.617–0.821). There was no difference in the expression of these six lncRNAs based on gender (p>0.05) or age (p>0.05).ConclusionsThese results suggest that the combined expression of six lncRNAs in PBMCs may serve as a potential biomarker for diagnosis and therapy response of MDD in the clinical setting.

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Section: Methodsmentioning

confidence: 99%

Long Non-Coding RNA: Potential Diagnostic and Therapeutic Biomarker for Major Depressive Disorder

Cui

Sun²,

Niu

et al. 2016

Med Sci Monit

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“…In general, the intermediary molecular events involve the pathways that are also activated in other forms of cardiac hypertrophic responses, such as pressure overload-induced cardiac hypertrophy. Accordingly, a multitude of pathways are perturbed, including expression and activation of trophic and mitotic factors, such as calcineurin, mitogen activated protein kinases, and transforming growth factor β pathways, as well as non-coding RNA and epigenetic factors 40, 118–125126, 127 . The characteristics of the molecular responses, while generally similar, vary according to the biological functions of genes carrying the causal mutations 125, 128, 129 .…”

Section: Pathogenesismentioning

confidence: 99%

Hypertrophic Cardiomyopathy

Marian

Braunwald

2017

Circulation Research

968

533

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Hypertrophic cardiomyopathy (HCM) is a genetic disorder that is characterized by left ventricular hypertrophy unexplained by secondary causes, and a non-dilated left ventricle with preserved or increased ejection fraction. It is commonly asymmetric with the most severe hypertrophy involving the basal interventricular septum. Left ventricular outflow tract obstruction is present at rest in about one third of the patients, and can be provoked in another third. The histologic features of HCM include myocyte hypertrophy and disarray, as well as interstitial fibrosis. The hypertrophy is also frequently associated with left ventricular diastolic dysfunction. In the majority of patients, HCM has a relatively benign course. However, HCM is also an important cause of sudden cardiac death, particularly in adolescents and young adults. Nonsustained ventricular tachycardia, syncope, a family history of sudden cardiac death, and severe cardiac hypertrophy are major risk factors for sudden cardiac death. This complication can usually be averted by implantation of a cardioverter-defibrillator in appropriate high-risk patients. Atrial fibrillation is also a common complication and is not well tolerated. Mutations in over a dozen genes encoding sarcomere-associated proteins cause HCM. MYH7 and MYBPC3, encoding β-myosin heavy chain and myosin binding protein C, respectively, are the two most common genes involved, together accounting for about 50% of the HCM families. In approximately 40% of HCM patients the causal genes remain to be identified. Mutations in genes responsible for storage diseases also cause a phenotype resembling HCM (genocopy or phenocopy). The routine applications of genetic testing and preclinical identification of family members represents an important advance. The genetic discoveries have enhanced understanding of the molecular pathogenesis of HCM and have stimulated efforts designed to identify new therapeutic agents.

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“…This includes genes that give rise to non-coding RNA, e.g. over 1,000 long non-coding RNAs have been found to be dysregulated in HCM [122], and various microRNAs involved in cardiac remodeling and regeneration [123,124]. As we have learned, new in vitro and in vivo models are also being generated at a steady pace, a process expedited through genome editing.…”

Section: Recent Advances In Crispr Genome Editing With Potential For mentioning

confidence: 99%

Genome Editing for the Understanding and Treatment of Cardiomyopathies

Nguyen¹,

Lim²,

Yokota³

2019

Preprint

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Cardiomyopathies are diseases of heart muscle, a significant percentage of which are genetic in origin. Cardiomyopathies can be classified as dilated, hypertrophic, restrictive, arrhythmogenic right ventricular or left ventricular non-compaction, although mixed morphologies are possible. A subset of neuromuscular disorders, notably Duchenne and Becker muscular dystrophies, are also characterized by cardiomyopathy aside from skeletal myopathy. The global burden of cardiomyopathies is certainly high, necessitating further research and novel therapies. Genome editing tools, which include zinc finger nucleases (ZFNs), transcription activator-like effector nucleases (TALENs) and clustered regularly interspaced short palindromic repeats (CRISPR) systems have emerged as increasingly important technologies in studying this group of cardiovascular disorders. In this review, we discuss the applications of genome editing in the understanding and treatment of cardiomyopathy. We also describe recent advances in genome editing that may help improve these applications, and some future prospects for genome editing in cardiomyopathy treatment.Keywords: dilated cardiomyopathy (DCM); hypertrophic cardiomyopathy (HCM); restrictive cardiomyopathy (RCM); arrhythmogenic right ventricular cardiomyopathy (ARVC); left ventricular non-compaction cardiomyopathy (LVNC); Duchenne muscular dystrophy; dystrophin; genome editing; CRISPR/Cas9; Cpf1 (Cas12a) Cardiomyopathy is also a major manifestation in a subset of neuromuscular disorders [7,8]. Cardiomyopathy is most commonly associated with Duchenne muscular dystrophy (DMD) and Becker muscular dystrophy (BMD), both X-linked recessive disorders caused by mutations in the dystrophin (DMD) gene [8]. DMD codes for dystrophin, a cytoskeletal protein that maintains the Preprints (www.preprints.org) | NOT PEER-REVIEWED | Posted: structural integrity of muscle fibres during contraction-relaxation cycles. Loss-of-function mutations in the DMD gene result in an absence of dystrophin, leading to DMD [9][10][11]. Mutations maintaining the DMD reading frame produce truncated but partly functional dystrophin, and often result in a milder form of the disease known as BMD [12,13]. Cardiomyopathy is a leading cause of death in both DMD and BMD patients and is routinely described as being DCM [13,14]. Other neuromuscular disorders associated with cardiomyopathy include the limb girdle muscle dystrophies, myotonic dystrophy, and Friedreich ataxia [15].Advances in molecular genetics enable genome editing to be incorporated into various fields of biomedical research, including the cardiovascular sciences. Currently, the most commonly used tools are zinc finger nucleases (ZFNs), transcription activator-like effector nucleases (TALENs), and clustered regularly interspaced short palindromic repeats (CRISPR) [16]. Both ZFNs and TALENs are engineered restriction enzymes created by combining a DNA binding domain with a DNA cleavage domain adapted from the FokI restriction enzyme [17][18][19]. The DNA binding domain in Z...

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Microarray profiling of long non-coding RNA (lncRNA) associated with hypertrophic cardiomyopathy

Cited by 52 publications

References 35 publications

Long Non-Coding RNA: Potential Diagnostic and Therapeutic Biomarker for Major Depressive Disorder

Long Non-Coding RNA: Potential Diagnostic and Therapeutic Biomarker for Major Depressive Disorder

Hypertrophic Cardiomyopathy

Genome Editing for the Understanding and Treatment of Cardiomyopathies

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