Martin Kenny

ORCID: 0000-0003-3055-8075
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About
Contact & Profiles
Research Areas
  • Platelet Disorders and Treatments
  • Blood properties and coagulation
  • Cell Adhesion Molecules Research
  • Spectroscopy and Chemometric Analyses
  • Venous Thromboembolism Diagnosis and Management
  • Spectroscopy Techniques in Biomedical and Chemical Research
  • Blood Coagulation and Thrombosis Mechanisms
  • Antiplatelet Therapy and Cardiovascular Diseases
  • Dialysis and Renal Disease Management
  • Gene Regulatory Network Analysis
  • Renal Transplantation Outcomes and Treatments
  • Erythrocyte Function and Pathophysiology
  • Molecular Biology Techniques and Applications
  • Periodontal Regeneration and Treatments
  • Extracellular vesicles in disease
  • Hemoglobin structure and function
  • Bioinformatics and Genomic Networks
  • Angiogenesis and VEGF in Cancer
  • Cell Image Analysis Techniques

University College Dublin
2023-2025

Royal College of Surgeons in Ireland
2017-2024

Sciences, Philosophie, Histoire
2023

Conway School of Landscape Design
2023

Breast cancer results in a three- to four-fold increased risk of venous thromboembolism (VTE), which is associated with reduced patient survival. Despite this, the mechanisms underpinning breast cancer-associated thrombosis remain poorly defined. Tumor cells can trigger endothelial cell (EC) activation resulting von Willebrand factor (VWF) secretion. Importantly, elevated plasma VWF levels constitute an independent biomarker for VTE risk. Moreover, model melanoma, treatment low molecular...

10.1111/jth.15794 article EN cc-by-nc Journal of Thrombosis and Haemostasis 2022-06-20

Spatial transcriptomics of histological sections have revolutionized research in life sciences and enabled unprecedented insights into genetic processes involved tissue reorganization. However, contrast to genomic analysis, the actual biomolecular composition sample has fallen behind, leaving a gap potentially highly valuable information. Raman microspectroscopy provides untargeted spatiomolecular information at high resolution, capable filling this gap. In study we demonstrate spatially...

10.1038/s41467-023-41417-0 article EN cc-by Nature Communications 2023-09-19

MYH9 -related disease patients with mutations in the contractile protein nonmuscle myosin heavy chain IIA display, among others, macrothrombocytopenia and a mild-to-moderate bleeding tendency. In this study, we used three mouse lines, each one point mutation Myh9 gene at positions 702, 1424, or 1841, to investigate mechanisms underlying increased risk. Agonist-induced activation of mutant platelets was comparable controls. However, light phosphorylation after reduced platelets, which...

10.1126/sciadv.abn2627 article EN cc-by-nc Science Advances 2022-05-18

ABSTRACT Purpose Multiple Sclerosis is an inflammatory neurodegenerative disease characterised by blood‐brain barrier dysfunction and leukocyte infiltration into the CNS. Platelets are best known for their contributions to haemostasis, however, upon activation, platelets release abundance of soluble vesicular‐associated proteins, termed platelet releasate (PR). This milieu contains numerous vasoactive that can attract leukocytes alter endothelial permeability. Experimental design We aimed...

10.1002/prca.202400019 article EN other-oa PROTEOMICS - CLINICAL APPLICATIONS 2025-01-20

Platelets interact with multiple adhesion proteins during thrombogenesis, yet little is known about their ability to assemble fibronectin matrix. In vitro three-dimensional superresolution microscopy complemented by biophysical and biochemical methods revealed fundamental insights into how platelet contractility drives fibrillogenesis. adhering thrombus (fibronectin fibrin) versus basement membrane components (laminin collagen IV) pull fibrils along apical underneath basal membrane,...

10.1126/sciadv.abj8331 article EN cc-by-nc Science Advances 2022-03-11

Abstract The initial contact with blood and its components, including plasma proteins platelets, directs the body's response to foreign materials. Natural scaffolds of extracellular matrix or fibrin contain fibrils nanoscale dimensions, but how platelets specifically respond topography architecture fibrous materials is still incompletely understood. Here, planar nanofiber are fabricated from native fibrinogen characterize morphology adherent activation markers for phosphatidylserine exposure...

10.1002/adhm.202200249 article EN Advanced Healthcare Materials 2022-05-08

Background: Active and passive biomechanical properties of platelets contribute substantially to thrombus formation.Actomyosin contractility drives clot contraction required for stabilizing the hemostatic plug.Impaired results in bleeding but is difficult detect using platelet function tests.Objectives: To determine how diminished myosin activity affects functions, including beyond contraction.Methods: Using IIA-specific pharmacologic inhibitor blebbistatin, we modulated from healthy donors...

10.1016/j.rpth.2024.102322 article EN cc-by Research and Practice in Thrombosis and Haemostasis 2024-01-01

Uraemic platelet dysfunction is not completely understood, in part due to non-physiological function assays. We have developed a physiological flow-based assay that quantifies microlitre volumes of blood under arterial shear. The aim this study was characterize before and after kidney transplantation. Ten patients scheduled for living donor transplant surgery nine healthy controls were analysed using the assay. motional parameters behaviour on von Willebrand factor (VWF) recorded customized...

10.1093/ckj/sfx148 article EN cc-by-nc Clinical Kidney Journal 2017-12-06

ABSTRACT Upon vascular injury, platelets are crucial for thrombus formation and contraction, but do they directly initiate early tissue repair processes? Using 3D super-resolution microscopy, micropost traction force specific integrin or myosin IIa inhibitors, we discovered here that form fibrillar adhesions. They assemble fibronectin nanofibrils using αIIbβ3 (CD41/CD61, GPIIb-IIIa) rather than α5β1 integrins, in contrast to fibroblasts. Highly contractile contact with proteins (fibronectin,...

10.1101/2020.04.20.050708 preprint EN cc-by-nd bioRxiv (Cold Spring Harbor Laboratory) 2020-04-20

Abstract MYH9-related disease patients with mutations in the contractile protein non-muscle myosin heavy chain IIA display, among others, macrothrombocytopenia and a mild to moderate bleeding tendency. In this study, we used three mouse lines, each one point mutation Myh9 gene at positions 702, 1424, or 1841, investigate mechanisms underlying increased risk. Agonist-induced activation of mutant platelets was comparable controls. However, light phosphorylation after reduced platelets, which...

10.1101/2021.11.10.468045 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2021-11-10
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