David Abraham

ORCID: 0000-0003-4249-9359
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About
Contact & Profiles
Research Areas
  • Systemic Sclerosis and Related Diseases
  • Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
  • Dermatologic Treatments and Research
  • Migration, Refugees, and Integration
  • Connective Tissue Growth Factor Research
  • Wound Healing and Treatments
  • Skin and Cellular Biology Research
  • Peripheral Artery Disease Management
  • Cell Adhesion Molecules Research
  • Mast cells and histamine
  • Political Philosophy and Ethics
  • Dermatological and Skeletal Disorders
  • Muscle metabolism and nutrition
  • Inflammatory Myopathies and Dermatomyositis
  • Diabetic Foot Ulcer Assessment and Management
  • Fibroblast Growth Factor Research
  • Nitric Oxide and Endothelin Effects
  • Erythropoietin and Anemia Treatment
  • Angiogenesis and VEGF in Cancer
  • Labor Movements and Unions
  • Autoimmune Bullous Skin Diseases
  • Pulmonary Hypertension Research and Treatments
  • Historical and Contemporary Political Dynamics
  • American Constitutional Law and Politics
  • Medical Imaging and Pathology Studies

University College London
2016-2025

The Royal Free Hospital
2014-2025

Universidade Federal do Amazonas
2025

University of Miami
2014-2024

Christ University
2024

British Society for Rheumatology
2023

Thomas Jefferson University
2021

UCL Biomedical Research Centre
2009-2018

Roland Hill (United Kingdom)
2003-2017

Bauhaus-Universität Weimar
2017

The hallmark of fibrotic processes is an excessive accumulation collagen. deposited collagen shows increase in pyridinoline cross-links, which are derived from hydroxylated lysine residues within the telopeptides. This change cross-linking related to irreversible tissues. cross-links likely be result increased activity enzyme responsible for hydroxylation telopeptides (telopeptide lysyl hydroxylase, or TLH). Although existence TLH has been postulated, gene encoding not identified. By...

10.1074/jbc.m307380200 article EN cc-by Journal of Biological Chemistry 2003-10-01

The endothelins are a family of endothelium-derived peptides that possess variety functions, including vasoconstriction. Endothelin-1 (ET-1) is up-regulated during tissue repair and promotes myofibroblast contraction migration, hence contributing to matrix remodeling repair. Here, we show addition ET-1 normal lung fibroblasts induces expression proteins contribute contractile phenotype, α-smooth muscle actin (α-SMA), ezrin, moesin, paxillin. We confirm enhances the ability contract...

10.1091/mbc.e03-12-0902 article EN Molecular Biology of the Cell 2004-03-30

Objective. Biomarkers of progression interstitial lung disease (ILD) are needed to allow early therapeutic intervention in patients with scleroderma-associated (SSc-ILD). Methods. A panel 8 serum cytokines [interleukin 6 (IL-6), IL-8, IL-10, CCL2, CXCL10, vascular endothelial growth factor, fibroblast factor 2, and CX3CL1] was assessed by Luminex bead technology exploratory cohorts 74 SSc 58 idiopathic pulmonary fibrosis (IPF). Mortality significant function decline [forced vital capacity...

10.3899/jrheum.120725 article EN The Journal of Rheumatology 2013-02-01

<h3>Background</h3> A polymorphism (rs35705950) 3 kb upstream of <i>MUC5B</i>, the gene encoding Mucin 5 subtype B, has been shown to be associated with familial and sporadic idiopathic pulmonary fibrosis (IPF). We set out verify whether this variant is also a risk factor for fibrotic lung disease in other settings confirm published findings UK Caucasian IPF population. <h3>Methods</h3> healthy controls (n=416) patients (n=110), sarcoidosis (n=180) systemic sclerosis (SSc) (n=440) were...

10.1136/thoraxjnl-2012-201786 article EN Thorax 2013-01-15

Systemic sclerosis (scleroderma) is a life-threatening autoimmune disease that characterized by the presence of specific autoantibodies and fibrosis skin major internal organs.We genotyped polymorphism (G-945C) in promoter connective-tissue growth factor (CTGF) gene 1000 subjects two groups: group 1, consisting 200 patients with systemic 188 control subjects; 2, 300 312 subjects. The combined groups represented an estimated 10% United Kingdom. We tested effect on transcription CTGF.The GG...

10.1056/nejmoa067655 article EN New England Journal of Medicine 2007-09-19

10.1016/0003-9861(62)90002-4 article EN Archives of Biochemistry and Biophysics 1962-11-01

Abstract Background Transforming growth factor beta (TGFβ), a multifunctional cytokine, plays crucial role in the accumulation of extracellular matrix components lung fibrosis, where fibroblasts are considered to play major role. Even though effects TGFβ on gene expression several proteins have been investigated fibroblast cell lines, global pattern response this cytokine adult is still unknown. Methods We used Affymetrix oligonucleotide microarrays U95v2, containing approximately 12,000...

10.1186/1465-9921-5-24 article EN cc-by Respiratory Research 2004-11-30

Abstract Platelet derived growth factor (PDGF) plays a pivotal role in the remodeling of connective tissues. Emerging data indicate distinctive PDGF receptor-α (PDGFRα) this process. In present study, Pdgfra gene was systemically inactivated adult mouse (α-KO mouse) and PDGFRα examined subcutaneously implanted sponge matrices. expressed fibroblasts -preserving control mice (Flox mice), significantly reduced sponges α-KO mice. Neovascularized areas were largely suppressed than Flox mice,...

10.1038/srep17948 article EN cc-by Scientific Reports 2015-12-07

Fibroblasts derived from the lungs of patients with idiopathic pulmonary fibrosis (IPF) and systemic sclerosis (SSc) produce low levels prostaglandin (PG) E2, due to a limited capacity up-regulate cyclooxygenase-2 (COX-2). This deficiency contributes functionally fibroproliferative state, however mechanisms responsible are incompletely understood. In present study, we examined whether reduced level COX-2 mRNA expression observed in fibrotic lung fibroblasts is regulated epigenetically. The...

10.1042/cs20150697 article EN cc-by Clinical Science 2016-01-08

Abstract Objective To investigate expression of the chemokine receptor CCR2 on key cell types involved in pathogenesis systemic sclerosis (SSc) and to assess potential for autocrine activation SSc dermal fibroblasts via CCL2/CCR2. Methods Chemokine skin biopsy tissues explanted from a well‐characterized cohort patients was examined using immunohistochemistry flow cytometry techniques. Autocrine regulation fibrotic markers CCR2+ fibroblast lines assessed specific ligand or antagonists....

10.1002/art.21396 article EN Arthritis & Rheumatism 2005-11-30

Abstract Objective To use a specific transforming growth factor β receptor type I (TGFβRI; activin receptor–like kinase 5 [ALK‐5]) inhibitor (SD208) to determine the role of activation TGFβRI (ALK‐5) in maintaining profibrotic phenotype dermal fibroblasts systemic sclerosis (SSc). Methods The effect SD208 on expression key biochemical markers fibrotic was compared cultured from clinically involved (lesional) and uninvolved skin patients with diffuse cutaneous SSc (dcSSc) healthy controls...

10.1002/art.21725 article EN Arthritis & Rheumatism 2006-03-30

&lt;i&gt;Background/Aims:&lt;/i&gt; The saphenous vein is commonly used for coronary artery bypass surgery but its patency poor. Vascular damage occurs during conventional surgery. However, improves when the graft harvested with minimal surgical trauma, partly due to preservation of vascular endothelial nitric oxide synthase (eNOS) and tissue sources (NO), a factor possessing both dilatory anti-proliferative properties. Apart from these grafts exhibiting an intact luminal endothelium they...

10.1159/000099833 article EN Journal of Vascular Research 2007-01-01

Systemic sclerosis (SSc) fibroblasts remain activated even in the absence of exogenous stimuli. Epigenetic alterations are thought to play a role for this endogenous activation. Trimethylation histone H3 on lysine 27 (H3K27me3) is regulated by Jumonji domain-containing protein 3 (JMJD3) and ubiquitously transcribed tetratricopeptide repeat chromosome X (UTX) therapeutically targetable manner. The aim study was explore H3K27me3 demethylases as potential targets treatment fibrosis.JMJD3...

10.1136/annrheumdis-2017-211501 article EN Annals of the Rheumatic Diseases 2017-10-25
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