A5035215947- Cardiomyopathy and Myosin Studies
- RNA modifications and cancer
- Viral Infections and Immunology Research
- Cancer-related molecular mechanisms research
- RNA Research and Splicing
- Cardiovascular Effects of Exercise
- Angiogenesis and VEGF in Cancer
- Eosinophilic Disorders and Syndromes
- Mesenchymal stem cell research
- interferon and immune responses
- Health and Medical Research Impacts
- Genomics and Chromatin Dynamics
- Circular RNAs in diseases
- Wound Healing and Treatments
- TGF-β signaling in diseases
- Coronary Interventions and Diagnostics
- Congenital heart defects research
- NF-κB Signaling Pathways
- MicroRNA in disease regulation
The University of Texas Health Science Center at Houston
2023-2024
University of Edinburgh
2018-2021
The Queen's Medical Research Institute
2021
British Heart Foundation
2018-2020
Queen's Medical Centre
2020
University of Glasgow
2020
Abstract Aims An intrinsic feature of gene transcription is the formation DNA superhelices near bubble, which are resolved upon induction transient double-stranded breaks (DSBs) by topoisomerases. Unrepaired DSBs pathogenic as they lead to cell cycle arrest, senescence, inflammation, and organ dysfunction. We posit that would be more prevalent at genomic sites associated with expression. The objectives were identify characterize genome-wide nucleotide resolution determine association in...
Transforming growth factor beta (TGF-β) is crucial for regulation of the endothelial cell (EC) homeostasis. Perturbation TGF-β signaling leads to pathological conditions in vasculature, causing cardiovascular disease and fibrotic disorders. The pathway critical endothelial-to-mesenchymal transition (EndMT), but a gap remains our understanding related endothelium. This study applied gain- loss-of function approach an vivo model skin wound healing demonstrate that miR-148b regulates has key...
The genome is constantly exposed to numerous stressors that induce DNA lesions, including double-stranded breaks (DSBs). DSBs are the most dangerous, as they genomic instability. In response damage, cell activates nuclear damage (DDR) and cytosolic sensing protein (CDSP) pathways, latter upon release of cytosol. CDSP pathway factor kappa B(NFκB) interferon regulatory 3 (IRF3) induces expression pro-inflammatory genes. There scant data on activation in human hearts with dilated cardiomyopathy...
Mutations in the DSP gene encoding desmoplakin, a constituent of desmosomes at intercalated discs (IDs), cause phenotype that spans arrhythmogenic cardiomyopathy (ACM) and dilated cardiomyopathy. It is typically characterized by biventricular enlargement dysfunction, myocardial fibrosis, cell death, arrhythmias. The canonical wingless-related integration (cWNT)/β-catenin pathway implicated pathogenesis ACM. β-catenin an indispensable co-transcriptional regulator cWNT member IDs. We...
Following myocardial infarction (MI), the adult heart has minimal regenerative potential. Conversely, neonatal can undergo extensive regeneration, and neovascularization capacity was hypothesized to contribute this difference. Here, we demonstrate higher angiogenic potential of compared with mouse cardiac endothelial cells (MCECs) in vitro use difference identify candidate microRNAs (miRs) regulating angiogenesis after MI. miR expression profiling revealed miR-96 miR-183 upregulation MCECs....
Background: An intrinsic feature of gene transcription is the formation DNA superhelices near bubble, which are resolved upon induction transient double-stranded breaks (DSBs) by topoisomerases. Unrepaired DSBs pathogenic as they lead to cell cycle arrest, senescence, inflammation, and organ dysfunction. Hypothesis Aims: We posit that would be more prevalent at genomic sites associated with expression. As Lamin-A (LMNA) regulates active through Lamin domains (LADS) we predict for common in...
ABSTRACT Aim Mutations in the DSP gene encoding desmoplakin, a constituent of desmosomes at intercalated discs (IDs), cause phenotype that spans arrhythmogenic cardiomyopathy (ACM) and dilated (DCM). It is typically characterized by biventricular enlargement dysfunction, severe myocardial fibrosis, cell death, arrhythmias. The canonical WNT (cWNT)/β-catenin signaling pathway implicated pathogenesis ACM. Given β-catenin, an indispensable co-transcriptional regulator cWNT pathway, also member...