A5067574993- Cancer, Hypoxia, and Metabolism
- Lipid metabolism and disorders
- Cancer, Lipids, and Metabolism
- TGF-β signaling in diseases
- Cell Adhesion Molecules Research
- Myasthenia Gravis and Thymoma
- Muscle Physiology and Disorders
- Cellular Mechanics and Interactions
- Cerebrovascular and genetic disorders
- Barrier Structure and Function Studies
- Angiogenesis and VEGF in Cancer
- Neuroinflammation and Neurodegeneration Mechanisms
- Diet and metabolism studies
- Bone health and treatments
- Bone Metabolism and Diseases
- Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
- Immune Response and Inflammation
- Research Data Management Practices
- Molecular Biology Techniques and Applications
- Distributed and Parallel Computing Systems
- Nonmelanoma Skin Cancer Studies
- Peripheral Neuropathies and Disorders
- Scientific Computing and Data Management
- Peripheral Nerve Disorders
- Neuroscience and Neuropharmacology Research
University of Oulu
2015-2024
Louisiana State University
2003
Human subjects consuming fish oil showed a significant suppression of cyclooxygenase-2 (COX-2) expression in blood monocytes when stimulated vitro with lipopolysaccharide (LPS), an agonist for Toll-like receptor 4 (TLR4). Results murine monocytic cell line (RAW 264.7) stably transfected COX-2 promoter reporter gene also demonstrated that LPS-induced was preferentially inhibited by docosahexaenoic acid (DHA, C22:6n-3) and eicosapentaenoic (EPA, C20:5n-3), the major n-3 polyunsaturated fatty...
Collagen type XVIII (COL18) is an abundant heparan sulfate proteoglycan in vascular basement membranes. Here, we asked (i) if the loss of COL18 would result blood-brain barrier (BBB) breakdown, pathological alterations small arteries and capillaries neuroinflammation as found cerebral vessel disease (CSVD) (ii) such changes may be associated with remodeling synapses neural extracellular matrix (ECM). We that 5-month-old Col18a1
Both transmembrane and extracellular cues, one of which is collagen XIII, regulate the formation function neuromuscular synapse, their absence results in myasthenia. We show that phenotypical changes XIII knock-out mice are milder than symptoms human patients, but Col13a1-/- recapitulate major muscle findings congenital myasthenic syndrome type 19 serve as a disease model. In lack synapses do not reach full size, alignment, complexity resulting reduced strength. Collagen particularly...
Collagen XIII occurs as both a transmembrane-bound and shed extracellular protein is able to regulate the formation function of neuromuscular synapses. Its absence results in myasthenia: presynaptic postsynaptic defects at junction (NMJ), leading destabilization motor nerves, muscle regeneration atrophy. Mutations COL13A1 have recently been found cause congenital myasthenic syndrome, characterized by fatigue chronic weakness, which may be lethal. We show here that collagen XIII-deficient...
Abstract Collagen XIII is a conserved transmembrane collagen mainly expressed in mesenchymal tissues. Previously, we have shown that modulates tissue development and homeostasis. Integrins are family of receptors mediate signals from the environment into cells vice versa. Integrin α11β1 receptor known to recognize GFOGER (O=hydroxyproline) sequence collagens. Interestingly, integrin both role regulation bone To study whether for XIII, utilized C2C12 transfected express as their only...
Basement membrane (BM) zone-associated collagen XV (ColXV) has been shown to suppress the malignancy of tumour cells, and its restin domain can inhibit angiogenesis. In human breast cancer, as well in many other carcinomas, ColXV is lost from epithelial BM zone prior invasion. Here, we addressed roles carcinogenesis using transgenic MMTV-PyMT mouse mammary carcinoma model. We show here for first time that inactivation Col15a1 mice leads changes fibrillar matrix increased growth. expressed by...
Transmembrane collagen XIII has been linked to maturation of the musculoskeletal system. Its absence in mice (Col13a1-/- ) results impaired neuromuscular junction (NMJ) differentiation and function, while transgenic overexpression (Col13a1oe leads abnormally high bone mass. Similarly, loss-of-function mutations COL13A1 humans produce muscle weakness, decreased motor synapse function mild dysmorphic skeletal features. Here, analysis exogenous various muscles revealed highly increased...
ABSTRACT Introduction : Evaluation of the nerve fascicular structure can be useful in diagnosing damage, but it is a very challenging task with 3T MRI because limited resolution. In this pilot study, we present feasibility high‐resolution 7T for examining structure. Methods A 3‐dimensional (3D) gradient‐spoiled sequence was used imaging peripheral nerves extremities. Images acquired different in‐plane resolutions (0.42 × 0.42 mm vs. 0.12 mm), and main field strengths (7T 3T) were compared....
Mutations in the COL13A1 gene result congenital myasthenic syndrome type 19 (CMS19), a disease of neuromuscular synapses and including various skeletal manifestations, particularly facial dysmorphisms. The phenotypic consequences Col13a1 null mice (Col13a1-/-) recapitulate muscle findings CMS19 patients. Collagen XIII (ColXIII) is exists as two forms, transmembrane protein soluble molecule. While Col13a1-/- have poorly formed junctions, prevention shedding ColXIII ectodomain Col13a1tm/tm...
Background Collagen XIII is a transmembrane collagen associated with neuromuscular junction development, and in humans its deficiency results congenital myasthenic syndrome type 19 (CMS19), which leads to breathing difficulties. CMS19 patients usually have restricted lung capacity one patient developed chronic disease. In single-cell RNA sequencing studies, has been identified as marker for pulmonary lipofibroblasts, implicated the resolution of fibrosis. Methods We investigated location...
Idiopathic pulmonary fibrosis (IPF) is a severe lung disease with poor prognosis and few treatment options. In the most widely used experimental model for this disease, bleomycin administered into lungs of mice, causing reaction inflammation consequent that resembles progression human IPF. The together induce changes in gene expression can be analyzed reverse transcription quantitative real-time PCR (RT-qPCR), which accurate normalization set stably expressed reference genes critical...
Abstract Collagen XVIII (COL18A1) is an abundant heparan sulfate proteoglycan in vascular basement membranes. Here, we asked (i) if the loss of collagen would result blood-brain barrier (BBB) breakdown, pathological alterations small arteries and capillaries neuroinflammation as found cerebral vessel disease (CSVD) (ii) such changes may be associated with remodeling synapses neural extracellular matrix (ECM). We that 5-month-old Col18a1 -/- mice had elevated BBB permeability for mouse IgG...
Antibodies against collagen XIII have previously been identified in patients with active thyroid-associated ophthalmopathy (TAO). Although expression has described extraocular muscles and orbital fat, its detailed localization thyroid tissues the connection to autoimmunity for remain unclear. Our objective was map potential targets these antibodies of orbit thyroid.
Abstract Fibrosis, neurodegeneration and cerebral angiomatosis (FINCA) is a childhood-onset multi-organ neurodevelopmental disorder associated with manifestations recurrent infections. The disease caused by variants in NHLRC2 initiating cascade of unknown pathological events. Previously, we have demonstrated that despite the significant decrease at molecular level, compound heterozygosity knock out p.Asp148Tyr alleles does not lead to severe phenotype mice. Here, analysed behavioural...
Searchable abstracts of presentations at key conferences on calcified tissues ISSN 2052-1219 (online)