A5039327438- Skin and Cellular Biology Research
- Cellular Mechanics and Interactions
- Nuclear Structure and Function
- Polysaccharides and Plant Cell Walls
- RNA Research and Splicing
- Congenital heart defects research
- Nail Diseases and Treatments
- Renal and related cancers
- Cardiovascular, Neuropeptides, and Oxidative Stress Research
- Angiogenesis and VEGF in Cancer
- Axon Guidance and Neuronal Signaling
- Mechanisms of cancer metastasis
- Cerebrovascular and genetic disorders
- Muscle Physiology and Disorders
- DNA Repair Mechanisms
- Wnt/β-catenin signaling in development and cancer
- Genetics, Aging, and Longevity in Model Organisms
- Virus-based gene therapy research
- Plant Reproductive Biology
- Developmental Biology and Gene Regulation
- Cardiovascular Disease and Adiposity
- Nitric Oxide and Endothelin Effects
- Apelin-related biomedical research
- Retinoids in leukemia and cellular processes
- Estrogen and related hormone effects
Medical University of Vienna
2005-2024
University of Vienna
2004-2023
Vienna Biocenter
2004-2022
Max Perutz Labs
2005-2022
BOKU University
2018-2019
Aging is a major risk factor for impaired cardiovascular health. Because the aging myocardium characterized by microcirculatory dysfunction, and because nerves align with vessels, we assessed impact of on cardiac neurovascular interface. We report that reduces nerve density in ventricle dysregulates vascular-derived neuroregulatory genes. down-regulates microRNA 145 (miR-145) derepresses neurorepulsive semaphorin-3A. miR-145 deletion, which increased
Plectin is a major intermediate filament (IF)-based cytolinker protein that stabilizes cells and tissues mechanically, regulates actin dynamics, serves as scaffolding platform for signaling molecules. In this study, we show plectin deficiency cause of aberrant keratin cytoskeleton organization caused by lack orthogonal IF cross-linking. Keratin networks in plectin-deficient were more susceptible to osmotic shock-induced retraction from peripheral areas, their okadaic acid-induced disruption...
Integrin-based mechanotransduction involves a complex focal adhesion (FA)-associated machinery that is able to detect and respond forces exerted either through components of the extracellular matrix or intracellular contractile actomyosin network. Here, we show hitherto unrecognized regulatory role vimentin intermediate filaments (IFs) in this process. By studying fibroblasts which IFs were decoupled from FAs, because deficiency (V0) loss network anchorage due cytolinker protein plectin...
Hutchinson-Gilford progeria syndrome (HGPS) is a premature aging disorder characterized by accelerated cardiovascular disease with extensive fibrosis. It caused mutation in LMNA leading to expression of truncated prelamin A (progerin) the nucleus. To investigate contribution endothelium HGPS pathology, we generated an endothelium-specific mouse model selective endothelial progerin expression. Transgenic mice develop interstitial myocardial and perivascular fibrosis left ventricular...
Mutations in the cytoskeletal linker protein plectin result multisystemic diseases affecting skin and muscle with indications of additional vascular system involvement. To study mechanisms underlying disorders, we established plectin-deficient endothelial cell mouse models. We show that apart from perturbing vimentin cytoskeleton cells, deficiency leads to severe distortions adherens junctions (AJs) as well tight junctions, accompanied by an upregulation actin stress fibres increased...
Abstract Age‐induced decline in osteogenic potential of bone marrow mesenchymal stem cells (BMSCs) potentiates osteoporosis and increases the risk for fractures. Despite epidemiology studies reporting concurrent development vascular diseases elderly, underlying mechanisms vascular‐bone cross‐talk aging are largely unknown. In this study, we show that accelerated endothelial deteriorates tissue through paracrine repression Wnt‐driven‐axis BMSCs. Here, utilize physiologically aged mice...
Agonist-induced translocation of protein kinase C (PKC) isozymes is mediated by receptors for the activated form kinase, shuttling it from one intracellular site to another and enhancing its catalytic activity. It however unknown whether themselves are anchored certain structures prior their engagement with PKC. We show here sequestering receptor 1 (RACK1) cytoskeleton through cytoskeletal linker plectin during initial stages cell adhesion. found that upon PKC activation, RACK1 was released...
According to current views the major hallmarks of physiological aging may be subdivided into three categories, primary causes cellular damage (genomic instability, telomere attrition, loss proteostasis, epigenetic alterations and compromised macroautophagy), antagonistic that represent response (deregulated nutrient sensing, senescence, mitochondrial dysfunction) integrative culprits phenotype (stem cell exhaustion, altered intercellular communication, chronic inflammation, dysbiosis). In...
Endothelial defects significantly contribute to cardiovascular pathology in the premature aging disease Hutchinson-Gilford progeria syndrome (HGPS). Using an endothelium-specific mouse model, we identify a novel, microRNA (miR) signature linked p53-senescence pathway and senescence-associated secretory phenotype (SASP). Progerin-expressing endothelial cells exert profound cell-non-autonomous effects initiating senescence non-endothelial cell populations causing immune infiltrates around...
Plectin, a typical cytolinker protein, is essential for skin and skeletal muscle integrity. It stabilizes cells mechanically, regulates cytoskeleton dynamics, serves as scaffolding platform signaling molecules. A variety of isoforms expressed in different tissues cell types account this versatility. To uncover the role plectin 1, major isoform mesenchymal origin, against background all other variants, we raised 1-specific antibodies generated isoform-deficient mice. In contrast to...
Mutations in the cytoskeletal linker protein plectin result multisystemic diseases affecting skin and muscle with indications of additional vascular system involvement. To study mechanisms underlying disorders, we established plectin-deficient endothelial cell mouse models. We show that apart from perturbing vimentin cytoskeleton cells, deficiency leads to severe distortions adherens junctions (AJs), as well tight junctions, accompanied by an upregulation actin stress fibres increased...
Abstract Aging is a major risk factor for impaired cardiovascular function. The aging heart characterized by vascular dysfunction, increased hypertrophy, fibrosis and electrophysiological alterations. Studies show endothelial cell (EC) function associates with senescence in aging. Since vessels nerves align, this interplay critical tissue homeostasis, we studied whether an impairment of the neuro-vascular interface may contribute to age-associated pathologies heart. To study innervation...
Aging is a major risk factor for impaired cardiovascular function. The aging heart characterized by vascular dysfunction, increased hypertrophy, fibrosis and electrophysiological alterations. However, the interaction between different age-associated changes in cardiac remodelling poorly define. Since vessels are aligned with nerves, this interplay critical tissue homeostasis, we investigated whether an impairment of neuro-vascular interface may contribute to pathologies heart. We show that...
Abstract Aging is a major risk factor for impaired cardiovascular health. The aging myocardium characterized by electrophysiological dysfunctions such as reduced heart rate variability. These alterations can be intrinsic within cardiomyocytes, but might modulated the cardiac autonomic nervous system, well 1 . It known that nerves align with vessels during development 2 , impact of on neuro-vascular interface unknown. Here, we report reduces nerve density specifically in left ventricle and...