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Cells, Volume 3, Issue 3 (September 2014), Pages 662-938

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Research

Jump to: Review, Other

Open AccessArticle Condensins are Required for Maintenance of Nuclear Architecture
Cells 2014, 3(3), 865-882; doi:10.3390/cells3030865
Received: 26 April 2014 / Revised: 20 June 2014 / Accepted: 11 August 2014 / Published: 22 August 2014
Cited by 5 | PDF Full-text (2158 KB) | HTML Full-text | XML Full-text
Abstract
The 3-dimensional spatial organization of eukaryotic genomes is important for regulation of gene expression as well as DNA damage repair. It has been proposed that one basic biophysical property of all nuclei is that interphase chromatin must be kept in a condensed prestressed
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The 3-dimensional spatial organization of eukaryotic genomes is important for regulation of gene expression as well as DNA damage repair. It has been proposed that one basic biophysical property of all nuclei is that interphase chromatin must be kept in a condensed prestressed state in order to prevent entropic pressure of the DNA polymer from expanding and disrupting the nuclear envelope. Although many factors can contribute to specific organizational states to compact chromatin, the mechanisms through which such interphase chromatin compaction is maintained are not clearly understood. Condensin proteins are known to exert compaction forces on chromosomes in anticipation of mitosis, but it is not known whether condensins also function to maintain interphase prestressed chromatin states. Here we show that RNAi depletion of the N-CAP-H2, N-CAP-D3 and SMC2 subunits of human condensin II leads to dramatic disruption of nuclear architecture and nuclear size. This is consistent with the idea that condensin mediated chromatin compaction contributes significantly to the prestressed condensed state of the interphase nucleus, and when such compaction forces are disrupted nuclear size and shape change due to chromatin expansion. Full article

Review

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Open AccessReview TRPV Channels in Mast Cells as a Target for Low-Level-Laser Therapy
Cells 2014, 3(3), 662-673; doi:10.3390/cells3030662
Received: 5 May 2014 / Revised: 9 June 2014 / Accepted: 17 June 2014 / Published: 26 June 2014
Cited by 6 | PDF Full-text (409 KB) | HTML Full-text | XML Full-text
Abstract
Low-level laser irradiation in the visible as well as infrared range is applied to skin for treatment of various diseases. Here we summarize and discuss effects of laser irradiation on mast cells that leads to degranulation of the cells. This process may contribute
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Low-level laser irradiation in the visible as well as infrared range is applied to skin for treatment of various diseases. Here we summarize and discuss effects of laser irradiation on mast cells that leads to degranulation of the cells. This process may contribute to initial steps in the final medical effects. We suggest that activation of TRPV channels in the mast cells forms a basis for the underlying mechanisms and that released ATP and histamine may be putative mediators for therapeutic effects. Full article
(This article belongs to the Special Issue Transient Receptor Potential (TRP) Channels)
Open AccessReview Mechanisms of Generating Polyubiquitin Chains of Different Topology
Cells 2014, 3(3), 674-689; doi:10.3390/cells3030674
Received: 13 May 2014 / Revised: 11 June 2014 / Accepted: 19 June 2014 / Published: 1 July 2014
Cited by 6 | PDF Full-text (940 KB) | HTML Full-text | XML Full-text
Abstract
Ubiquitination is an important post-translational process involving attachment of the ubiquitin molecule to lysine residue/s on a substrate protein or on another ubiquitin molecule, leading to the formation of protein mono-, multi- or polyubiquitination. Protein ubiquitination requires a cascade of three enzymes, where
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Ubiquitination is an important post-translational process involving attachment of the ubiquitin molecule to lysine residue/s on a substrate protein or on another ubiquitin molecule, leading to the formation of protein mono-, multi- or polyubiquitination. Protein ubiquitination requires a cascade of three enzymes, where the interplay between different ubiquitin-conjugating and ubiquitin-ligase enzymes generates diverse ubiquitinated proteins topologies. Structurally diverse ubiquitin conjugates are recognized by specific proteins with ubiquitin-binding domains (UBDs) to target the substrate proteins of different pathways. The mechanism/s for generating the different ubiquitinated proteins topologies is not well understood. Here, we will discuss our current understanding of the mechanisms underpinning the generation of mono- or polyubiquitinated substrates. In addition, we will discuss how linkage-specific polyubiquitin chains through lysines-11, -48 or -63 are formed to target proteins to different fates by binding specific UBD proteins. Full article
(This article belongs to the Special Issue Protein Ubiquitination)
Open AccessReview Ubiquitin Signaling: Extreme Conservation as a Source of Diversity
Cells 2014, 3(3), 690-701; doi:10.3390/cells3030690
Received: 20 March 2014 / Revised: 20 June 2014 / Accepted: 1 July 2014 / Published: 10 July 2014
Cited by 1 | PDF Full-text (646 KB) | HTML Full-text | XML Full-text
Abstract
Around 2 × 103–2.5 × 103 million years ago, a unicellular organism with radically novel features, ancestor of all eukaryotes, dwelt the earth. This organism, commonly referred as the last eukaryotic common ancestor, contained in its proteome the same
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Around 2 × 103–2.5 × 103 million years ago, a unicellular organism with radically novel features, ancestor of all eukaryotes, dwelt the earth. This organism, commonly referred as the last eukaryotic common ancestor, contained in its proteome the same functionally capable ubiquitin molecule that all eukaryotic species contain today. The fact that ubiquitin protein has virtually not changed during all eukaryotic evolution contrasts with the high expansion of the ubiquitin system, constituted by hundreds of enzymes, ubiquitin-interacting proteins, protein complexes, and cofactors. Interestingly, the simplest genetic arrangement encoding a fully-equipped ubiquitin signaling system is constituted by five genes organized in an operon-like cluster, and is found in archaea. How did ubiquitin achieve the status of central element in eukaryotic physiology? We analyze here the features of the ubiquitin molecule and the network that it conforms, and propose notions to explain the complexity of the ubiquitin signaling system in eukaryotic cells. Full article
(This article belongs to the Special Issue Protein Ubiquitination)
Figures

Open AccessReview MicroRNAs Control Macrophage Formation and Activation: The Inflammatory Link between Obesity and Cardiovascular Diseases
Cells 2014, 3(3), 702-712; doi:10.3390/cells3030702
Received: 29 May 2014 / Revised: 27 June 2014 / Accepted: 1 July 2014 / Published: 10 July 2014
Cited by 6 | PDF Full-text (301 KB) | HTML Full-text | XML Full-text
Abstract
Activation and recruitment of resident macrophages in tissues in response to physiological stress are crucial regulatory processes in promoting the development of obesity-associated metabolic disorders and cardiovascular diseases. Recent studies have provided compelling evidence that microRNAs play important roles in modulating monocyte formation,
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Activation and recruitment of resident macrophages in tissues in response to physiological stress are crucial regulatory processes in promoting the development of obesity-associated metabolic disorders and cardiovascular diseases. Recent studies have provided compelling evidence that microRNAs play important roles in modulating monocyte formation, macrophage maturation, infiltration into tissues and activation. Macrophage-dependent systemic physiological and tissue-specific responses also involve cell-cell interactions between macrophages and host tissue niche cell components, including other tissue-resident immune cell lineages, adipocytes, vascular smooth muscle and others. In this review, we highlight the roles of microRNAs in regulating the development and function of macrophages in the context of obesity, which could provide insights into the pathogenesis of obesity-related metabolic syndrome and cardiovascular diseases. Full article
(This article belongs to the Special Issue MicroRNAs in Cardiovascular Biology and Disease)
Open AccessReview MiRiad Roles for MicroRNAs in Cardiac Development and Regeneration
Cells 2014, 3(3), 724-750; doi:10.3390/cells3030724
Received: 29 May 2014 / Revised: 25 June 2014 / Accepted: 8 July 2014 / Published: 22 July 2014
Cited by 6 | PDF Full-text (1046 KB) | HTML Full-text | XML Full-text
Abstract
Cardiac development is an exquisitely regulated process that is sensitive to perturbations in transcriptional activity and gene dosage. Accordingly, congenital heart abnormalities are prevalent worldwide, and are estimated to occur in approximately 1% of live births. Recently, small non-coding RNAs, known as microRNAs,
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Cardiac development is an exquisitely regulated process that is sensitive to perturbations in transcriptional activity and gene dosage. Accordingly, congenital heart abnormalities are prevalent worldwide, and are estimated to occur in approximately 1% of live births. Recently, small non-coding RNAs, known as microRNAs, have emerged as critical components of the cardiogenic regulatory network, and have been shown to play numerous roles in the growth, differentiation, and morphogenesis of the developing heart. Moreover, the importance of miRNA function in cardiac development has facilitated the identification of prospective therapeutic targets for patients with congenital and acquired cardiac diseases. Here, we discuss findings attesting to the critical role of miRNAs in cardiogenesis and cardiac regeneration, and present evidence regarding the therapeutic potential of miRNAs for cardiovascular diseases. Full article
(This article belongs to the Special Issue MicroRNAs in Cardiovascular Biology and Disease)
Open AccessReview Cellular and Developmental Biology of TRPM7 Channel-Kinase: Implicated Roles in Cancer
Cells 2014, 3(3), 751-777; doi:10.3390/cells3030751
Received: 10 March 2014 / Revised: 15 July 2014 / Accepted: 15 July 2014 / Published: 30 July 2014
Cited by 7 | PDF Full-text (1104 KB) | HTML Full-text | XML Full-text
Abstract
The transient receptor potential melastatin-subfamily member 7 (TRPM7) is a ubiquitously expressed cation-permeable ion channel with intrinsic kinase activity that plays important roles in various physiological functions. Biochemical and electrophysiological studies, in combination with molecular analyses of TRPM7, have generated insights into its
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The transient receptor potential melastatin-subfamily member 7 (TRPM7) is a ubiquitously expressed cation-permeable ion channel with intrinsic kinase activity that plays important roles in various physiological functions. Biochemical and electrophysiological studies, in combination with molecular analyses of TRPM7, have generated insights into its functions as a cellular sensor and transducer of physicochemical stimuli. Accumulating evidence indicates that TRPM7 channel-kinase is essential for cellular processes, such as proliferation, survival, differentiation, growth, and migration. Experimental studies in model organisms, such as zebrafish, mouse, and frog, have begun to elucidate the pleiotropic roles of TRPM7 during embryonic development from gastrulation to organogenesis. Aberrant expression and/or activity of the TRPM7 channel-kinase have been implicated in human diseases including a variety of cancer. Studying the functional roles of TRPM7 and the underlying mechanisms in normal cells and developmental processes is expected to help understand how TRPM7 channel-kinase contributes to pathogenesis, such as malignant neoplasia. On the other hand, studies of TRPM7 in diseases, particularly cancer, will help shed new light in the normal functions of TRPM7 under physiological conditions. In this article, we will provide an updated review of the structural features and biological functions of TRPM7, present a summary of current knowledge of its roles in development and cancer, and discuss the potential of TRPM7 as a clinical biomarker and therapeutic target in malignant diseases. Full article
(This article belongs to the Special Issue Transient Receptor Potential (TRP) Channels)
Figures

Open AccessReview MicroRNAs in the Stressed Heart: Sorting the Signal from the Noise
Cells 2014, 3(3), 778-801; doi:10.3390/cells3030778
Received: 12 June 2014 / Revised: 16 July 2014 / Accepted: 23 July 2014 / Published: 5 August 2014
Cited by 5 | PDF Full-text (750 KB) | HTML Full-text | XML Full-text
Abstract
The short noncoding RNAs, known as microRNAs, are of undisputed importance in cellular signaling during differentiation and development, and during adaptive and maladaptive responses of adult tissues, including those that comprise the heart. Cardiac microRNAs are regulated by hemodynamic overload resulting from exercise
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The short noncoding RNAs, known as microRNAs, are of undisputed importance in cellular signaling during differentiation and development, and during adaptive and maladaptive responses of adult tissues, including those that comprise the heart. Cardiac microRNAs are regulated by hemodynamic overload resulting from exercise or hypertension, in the response of surviving myocardium to myocardial infarction, and in response to environmental or systemic disruptions to homeostasis, such as those arising from diabetes. A large body of work has explored microRNA responses in both physiological and pathological contexts but there is still much to learn about their integrated actions on individual mRNAs and signaling pathways. This review will highlight key studies of microRNA regulation in cardiac stress and suggest possible approaches for more precise identification of microRNA targets, with a view to exploiting the resulting data for therapeutic purposes. Full article
(This article belongs to the Special Issue MicroRNAs in Cardiovascular Biology and Disease)
Open AccessReview microRNAs and Cardiac Cell Fate
Cells 2014, 3(3), 802-823; doi:10.3390/cells3030802
Received: 30 May 2014 / Revised: 16 July 2014 / Accepted: 17 July 2014 / Published: 5 August 2014
Cited by 5 | PDF Full-text (863 KB) | HTML Full-text | XML Full-text
Abstract
The role of small, non-coding microRNAs (miRNAs) has recently emerged as fundamental in the regulation of the physiology of the cardiovascular system. Several specific miRNAs were found to be expressed in embryonic, postnatal, and adult cardiac tissues. In the present review, we will
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The role of small, non-coding microRNAs (miRNAs) has recently emerged as fundamental in the regulation of the physiology of the cardiovascular system. Several specific miRNAs were found to be expressed in embryonic, postnatal, and adult cardiac tissues. In the present review, we will provide an overview about their role in controlling the different pathways regulating cell identity and fate determination. In particular, we will focus on the involvement of miRNAs in pluripotency determination and reprogramming, and specifically on cardiac lineage commitment and cell direct transdifferentiation into cardiomyocytes. The identification of cardiac-specific miRNAs and their targets provide new promising insights into the mechanisms that regulate cardiac development, function and dysfunction. Furthermore, due to their contribution in reprogramming, they could offer new opportunities for developing safe and efficient cell-based therapies for cardiovascular disorders. Full article
(This article belongs to the Special Issue MicroRNAs in Cardiovascular Biology and Disease)
Open AccessReview Regulation of Endoplasmic Reticulum-Associated Protein Degradation (ERAD) by Ubiquitin
Cells 2014, 3(3), 824-847; doi:10.3390/cells3030824
Received: 6 June 2014 / Revised: 9 July 2014 / Accepted: 20 July 2014 / Published: 5 August 2014
Cited by 22 | PDF Full-text (1284 KB) | HTML Full-text | XML Full-text
Abstract
Quality control of protein folding inside the endoplasmic reticulum (ER) includes chaperone-mediated assistance in folding and the selective targeting of terminally misfolded species to a pathway called ER-associated protein degradation, or simply ERAD. Once selected for ERAD, substrates will be transported (back) into
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Quality control of protein folding inside the endoplasmic reticulum (ER) includes chaperone-mediated assistance in folding and the selective targeting of terminally misfolded species to a pathway called ER-associated protein degradation, or simply ERAD. Once selected for ERAD, substrates will be transported (back) into the cytosol, a step called retrotranslocation. Although still ill defined, retrotranslocation likely involves a protein conducting channel that is in part formed by specific membrane-embedded E3 ubiquitin ligases. Early during retrotranslocation, reversible self-ubiquitination of these ligases is thought to aid in initiation of substrate transfer across the membrane. Once being at least partially exposed to the cytosol, substrates will become ubiquitinated on the cytosolic side of the ER membrane by the same E3 ubiquitin ligases. Ubiquitin on substrates was originally thought to be a permanent modification that (1) promotes late steps of retrotranslocation by recruiting the energy-providing ATPase Cdc48p/p97 via binding to its associated adaptor proteins and that (2) serves to target substrates to the proteasome. Recently it became evident, however, that the poly-ubiquitin chains (PUCs) on ERAD substrates are often subject to extensive remodeling, or processing, at several stages during ERAD. This review recapitulates the current knowledge and recent findings about PUC processing on ERAD substrates and ubiquitination of ERAD machinery components and discusses their functional consequences. Full article
(This article belongs to the Special Issue Protein Ubiquitination)
Figures

Open AccessReview Bacterial Effectors and Their Functions in the Ubiquitin-Proteasome System: Insight from the Modes of Substrate Recognition
Cells 2014, 3(3), 848-864; doi:10.3390/cells3030848
Received: 17 March 2014 / Revised: 12 July 2014 / Accepted: 21 July 2014 / Published: 18 August 2014
Cited by 4 | PDF Full-text (4984 KB) | HTML Full-text | XML Full-text
Abstract
Protein ubiquitination plays indispensable roles in the regulation of cell homeostasis and pathogenesis of neoplastic, infectious, and neurodegenerative diseases. Given the importance of this modification, it is to be expected that several pathogenic bacteria have developed the ability to utilize the host ubiquitin
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Protein ubiquitination plays indispensable roles in the regulation of cell homeostasis and pathogenesis of neoplastic, infectious, and neurodegenerative diseases. Given the importance of this modification, it is to be expected that several pathogenic bacteria have developed the ability to utilize the host ubiquitin system for their own benefit. Modulation of the host ubiquitin system by bacterial effector proteins inhibits innate immune responses and hijacks central signaling pathways. Bacterial effectors mimic enzymes of the host ubiquitin system, but may or may not be structurally similar to the mammalian enzymes. Other effectors bind and modify components of the host ubiquitin system, and some are themselves subject to ubiquitination. This review will describe recent findings, based on structural analyses, regarding how pathogens use post-translational modifications of proteins to establish an infection. Full article
(This article belongs to the Special Issue Protein Ubiquitination)
Open AccessReview Non-Coding RNAs Including miRNAs and lncRNAs in Cardiovascular Biology and Disease
Cells 2014, 3(3), 883-898; doi:10.3390/cells3030883
Received: 10 July 2014 / Revised: 15 August 2014 / Accepted: 15 August 2014 / Published: 22 August 2014
Cited by 15 | PDF Full-text (694 KB) | HTML Full-text | XML Full-text
Abstract
It has been recognized for decades that proteins, which are encoded by our genome and produced via transcription and translation steps, are building blocks that play vital roles in almost all biological processes. Mutations identified in many protein-coding genes are linked to various
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It has been recognized for decades that proteins, which are encoded by our genome and produced via transcription and translation steps, are building blocks that play vital roles in almost all biological processes. Mutations identified in many protein-coding genes are linked to various human diseases. However, this “protein-centered” dogma has been challenged in recent years with the discovery that the majority of our genome is “non-coding” yet transcribed. Non-coding RNA has become the focus of “next generation” biology. Here, we review the emerging field of non-coding RNAs, including microRNAs (miRNAs) and long non-coding RNAs (lncRNAs), and their role in cardiovascular function and disease. Full article
(This article belongs to the Special Issue MicroRNAs in Cardiovascular Biology and Disease)
Open AccessReview Roles of Calcium Regulating MicroRNAs in Cardiac Ischemia-Reperfusion Injury
Cells 2014, 3(3), 899-913; doi:10.3390/cells3030899
Received: 26 May 2014 / Revised: 2 September 2014 / Accepted: 3 September 2014 / Published: 11 September 2014
Cited by 5 | PDF Full-text (1407 KB) | HTML Full-text | XML Full-text
Abstract
Cardiac Ca2+ cycling and signaling are closely associated with cardiac function. Changes in cellular Ca2+ homeostasis may lead to aberrant cardiac rhythm and may play a critical role in the pathogenesis of cardiac diseases, due to their exacerbation of heart failure.
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Cardiac Ca2+ cycling and signaling are closely associated with cardiac function. Changes in cellular Ca2+ homeostasis may lead to aberrant cardiac rhythm and may play a critical role in the pathogenesis of cardiac diseases, due to their exacerbation of heart failure. MicroRNAs (miRNAs) play a key role in the regulation of gene expression at the post-transcriptional level and participate in regulating diverse biological processes. The emerging evidence indicates that the expression profiles of miRNAs vary among human diseases, including cardiovascular diseases. Cardiac Ca2+-handling and signaling proteins are also regulated by miRNAs. Given the relationship between cardiac Ca2+ homeostasis and signaling and miRNA, Ca2+-related miRNAs may serve as therapeutic targets during the treatment of heart failure. In this review, we summarize the knowledge currently available regarding the role of Ca2+ in cardiac function, as well as changes in Ca2+ cycling and homeostasis and the handling of these processes by miRNAs during cardiac ischemia-reperfusion injury. Full article
(This article belongs to the Special Issue MicroRNAs in Cardiovascular Biology and Disease)
Open AccessReview TRPV1 and Endocannabinoids: Emerging Molecular Signals that Modulate Mammalian Vision
Cells 2014, 3(3), 914-938; doi:10.3390/cells3030914
Received: 1 July 2014 / Revised: 27 August 2014 / Accepted: 5 September 2014 / Published: 12 September 2014
Cited by 6 | PDF Full-text (1231 KB) | HTML Full-text | XML Full-text
Abstract
Transient Receptor Potential Vanilloid 1 (TRPV1) subunits form a polymodal cation channel responsive to capsaicin, heat, acidity and endogenous metabolites of polyunsaturated fatty acids. While originally reported to serve as a pain and heat detector in the peripheral nervous system, TRPV1 has been
[...] Read more.
Transient Receptor Potential Vanilloid 1 (TRPV1) subunits form a polymodal cation channel responsive to capsaicin, heat, acidity and endogenous metabolites of polyunsaturated fatty acids. While originally reported to serve as a pain and heat detector in the peripheral nervous system, TRPV1 has been implicated in the modulation of blood flow and osmoregulation but also neurotransmission, postsynaptic neuronal excitability and synaptic plasticity within the central nervous system. In addition to its central role in nociception, evidence is accumulating that TRPV1 contributes to stimulus transduction and/or processing in other sensory modalities, including thermosensation, mechanotransduction and vision. For example, TRPV1, in conjunction with intrinsic cannabinoid signaling, might contribute to retinal ganglion cell (RGC) axonal transport and excitability, cytokine release from microglial cells and regulation of retinal vasculature. While excessive TRPV1 activity was proposed to induce RGC excitotoxicity, physiological TRPV1 activity might serve a neuroprotective function within the complex context of retinal endocannabinoid signaling. In this review we evaluate the current evidence for localization and function of TRPV1 channels within the mammalian retina and explore the potential interaction of this intriguing nociceptor with endogenous agonists and modulators. Full article
(This article belongs to the Special Issue Transient Receptor Potential (TRP) Channels)

Other

Jump to: Research, Review

Open AccessBrief Report MicroRNA-421 Dysregulation is Associated with Tetralogy of Fallot
Cells 2014, 3(3), 713-723; doi:10.3390/cells3030713
Received: 21 May 2014 / Revised: 2 July 2014 / Accepted: 3 July 2014 / Published: 11 July 2014
Cited by 5 | PDF Full-text (400 KB) | HTML Full-text | XML Full-text
Abstract
The importance of microRNAs for maintaining stability in the developing vertebrate heart has recently become apparent. In addition, there is a growing appreciation for the significance of microRNAs in developmental pathology, including the formation of congenital heart defects. We examined the expression of
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The importance of microRNAs for maintaining stability in the developing vertebrate heart has recently become apparent. In addition, there is a growing appreciation for the significance of microRNAs in developmental pathology, including the formation of congenital heart defects. We examined the expression of microRNAs in right ventricular (RV) myocardium from infants with idiopathic tetralogy of Fallot (TOF, without a 22q11.2 deletion), and found 61 microRNAs to be significantly changed in expression in myocardium from children with TOF compared to normally developing comparison subjects (O’Brien et al. 2012). Predicted targets of microRNAs with altered expression were enriched for gene networks that regulate cardiac development. We previously derived a list of 229 genes known to be critical to heart development, and found 44 had significantly changed expression in TOF myocardium relative to normally developing myocardium. These 44 genes had significant negative correlations with 33 microRNAs, each of which also had significantly changed expression. Here, we focus on miR-421, as it is significantly upregulated in RV tissue from infants with TOF; is predicted to interact with multiple members of cardiovascular regulatory pathways; and has been shown to regulate cell proliferation. We knocked down, and over expressed miR-421 in primary cells derived from the RV of infants with TOF, and infants with normally developing hearts, respectively. We found a significant inverse correlation between the expression of miR-421 and SOX4, a key regulator of the Notch pathway, which has been shown to be important for the cardiac outflow track. These findings suggest that the dysregulation of miR-421 warrants further investigation as a potential contributor to tetralogy of Fallot. Full article
(This article belongs to the Special Issue MicroRNAs in Cardiovascular Biology and Disease)

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