Special Issue "MicroRNAs in Cardiovascular Biology and Disease"
A special issue of Cells (ISSN 2073-4409).
Deadline for manuscript submissions: closed (30 May 2014)
Dr. Stephen Y. Chan
Divisions of Cardiovascular Medicine and Network Medicine, Department of Medicine Brigham and Women's Hospital, Harvard Medical School 77 Avenue Louis Pasteur, Room 630N Boston, MA 02115, USA
Phone: +1 617-525-4844
Fax: +1 617-525-4830
Interests: microRNA; network biology; pulmonary hypertension; hypoxia; mitochondrial metabolism; vascular biology
Since the initial discovery of microRNAs’ specific biological functions in the late 1990s, our understanding of these unique RNA molecules in both health and disease has grown exponentially. The impact of miRNA biology continues to be wide-reaching and often surprising—particularly in the field of cardiovascular physiology. Beyond the canonical functions of individual microRNAs that affect their isolated gene targets and downstream pathophenotypes, developing concepts in cardiovascular biology include the study of paracrine or endocrine functions of extracellular forms of microRNAs, an increasing appreciation for the complexity of regulation of microRNAs via other non-coding RNA molecules, and a growing interest in understanding the "network-based" pleiotropy of microRNAs through a combination of computational and experimental methods.
This special issue will provide an open access opportunity for publishing research work and review articles related to cardiovascular biology and disease, and to offer comprehensive new insights into the current and future directions of this exciting and important research field.
Dr. Stephen Y. Chan
Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. Papers will be published continuously (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.
Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are refereed through a peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed Open Access quarterly journal published by MDPI.
Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 500 CHF (Swiss Francs). English correction and/or formatting fees of 250 CHF (Swiss Francs) will be charged in certain cases for those articles accepted for publication that require extensive additional formatting and/or English corrections.
- cardiovascular biology and disease
- network biology
- circulating microRNA
- vascular biology
Cells 2014, 3(3), 724-750; doi:10.3390/cells3030724
Received: 29 May 2014; in revised form: 25 June 2014 / Accepted: 8 July 2014 / Published: 22 July 2014| PDF Full-text (1046 KB) | HTML Full-text | XML Full-text
Cells 2014, 3(3), 713-723; doi:10.3390/cells3030713
Received: 21 May 2014; in revised form: 2 July 2014 / Accepted: 3 July 2014 / Published: 11 July 2014| PDF Full-text (400 KB) | HTML Full-text | XML Full-text
Review: 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; in revised form: 27 June 2014 / Accepted: 1 July 2014 / Published: 10 July 2014| PDF Full-text (301 KB) | HTML Full-text | XML Full-text
The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.
Type of Paper: Article
Tentative Title: MicroRNA-421 Dysregulation Contributes to Tetralogy of Fallot
Authors: Douglas C. Bittel, Ph.D.1,*, Nataliya Kibiryeva, M.D.1, Jennifer A. Marshall MPH, RN, RRT, CCRC 1, Michael Artman M.D 2 and James E. O’Brien, Jr., M.D 1
Affiliations: 1 Ward Family Heart Center, Children’s Mercy Hospitals and Clinics and University of Missouri-Kansas City School of Medicine, Kansas, MO 64108, USA; * E-Mail: firstname.lastname@example.org
2 Department of Pediatrics, Children’s Mercy Hospitals and Clinics and University of Missouri-Kansas City School of Medicine, Kansas City, MO 64108, USA
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 for 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). The pattern of miRNA expression in TOF myocardium had a surprising resemblance to expression patterns in fetal myocardium. Predicted targets of microRNAs with altered expression were enriched for gene networks that regulate cardiac development. We 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 correlation with 33 microRNAs, each of which also had significantly changed expression. Here, we focus on miR-421 as it is significantly up regulated 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 overexpressed miR-421 in primary cells derived from RV from infants with TOF and infants with normally developing hearts, respectively. We found a negative correlation between the expression of miR-421 and several key genes in the WNT and Notch pathways. These finding suggest that the dysregulation of miR-421 in the developing human heart may contribute to tetralogy of Fallot and warrants further investigation.
Type of Paper: Review manuscript with some original data
Tentative Title: miRNAs as regulators of regulators: the complex knots of the homeobox transcription factor Pitx2
Authors: Francisco Hernandez-Torres, Houria Daimi, Estefania Lozano-Velasco, Ana Chinchilla, Jorge Nicolas Dominguez, Amelia Aranega and Diego Franco
Affiliations: Department of Experimental Biology, University of Jaen, 23071 Jaen, Spain
Abstract: The homeobox transcription factor Pitx2 plays a relevant role during early embryogenesis, as part of the left-right signaling cascade and more recently, a pivotal role for this transcription factor has been reported in cardiac and skeletal muscle development and disease. Pitx2 is dynamically expressed during embryogenesis and three distinct alternative spliced variants have been reported; Pitx2a, Pitx2b and Pitx2c. Although all Pitx2 isoforms are expressed during early gastrulation, Pitx2c is the most abundant isoform during muscle organogenesis. Over the last years we have gained insights into the transcriptional regulatory mechanisms driven by Pitx2 in both cardiac and skeletal muscle. Interestingly, besides playing a role in regulating a large number of protein-coding genes, microRNAs have also been reported to be regulated by Pitx2. In this review, we will summarize current state of-the-art knowledge about the regulatory mechanisms controlling Pitx2-microRNA interactions, and their link to muscle diseases and we will provide novel insights into microRNA-mediated regulatory networks controlling Pitx2 and their implication for therapeutics.
Last update: 16 January 2014