A5033306681- Ion channel regulation and function
- Cardiac electrophysiology and arrhythmias
- Nitric Oxide and Endothelin Effects
- Mitochondrial Function and Pathology
- Tryptophan and brain disorders
- Phosphodiesterase function and regulation
- Renal Diseases and Glomerulopathies
- Birth, Development, and Health
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Cancer, Hypoxia, and Metabolism
- Receptor Mechanisms and Signaling
- Ion Channels and Receptors
- Eicosanoids and Hypertension Pharmacology
- Protein Kinase Regulation and GTPase Signaling
- Telomeres, Telomerase, and Senescence
- Sirtuins and Resveratrol in Medicine
- Wnt/β-catenin signaling in development and cancer
- GDF15 and Related Biomarkers
- Neuroinflammation and Neurodegeneration Mechanisms
- Neuroscience and Neuropharmacology Research
- Sulfur Compounds in Biology
- Nicotinic Acetylcholine Receptors Study
- Calcium signaling and nucleotide metabolism
- Circadian rhythm and melatonin
- Metabolomics and Mass Spectrometry Studies
University of Fribourg
2021-2025
University of Bern
2018-2024
University of Pavia
2014-2015
Store-operated Ca 2+ entry (SOCE) is activated following depletion of the inositol-1,4,5-trisphosphate (InsP 3 )-sensitive pool to regulate proliferation in immortalized cell lines established from either primary or metastatic lesions. The molecular nature SOCE may involve both Stim1, which senses levels within endoplasmic reticulum (ER) reservoir, and a number -permeable channels on plasma membrane, including Orai1, Orai3, members canonical transient receptor (TRPC1–7) family ion channels....
During physical exercise or stress, the sympathetic system stimulates cardiac contractility via β-adrenergic receptor (β-AR) activation, resulting in protein kinase A (PKA)-mediated phosphorylation of ryanodine RyR2. PKA-dependent "hyperphosphorylation" RyR2 channel has been proposed as a major impairment that contributes to progression heart failure. However, sites PKA and their status diseases are not well defined. Among known sites, serine 2030 (S2030) remains highly controversial site...
Increased endothelial permeability plays an important role in blood-brain barrier (BBB) dysfunction and is implicated neuronal injury many diseased conditions. BBB disruption primarily determined by of cell-cell junctions. Deprivation oxygen supply or hypoxia, a common feature variety human diseases, major risk factor for disruption. The molecular regulatory mechanisms hypoxia-induced remain incompletely understood. mitochondrial enzyme, arginase type II (Arg-II), has been shown to promote...
Background Aberrant mitochondrial metabolism is a key source of massive reactive oxygen species (mtROS) in tumour cells. Arginase-II (Arg-II), widely expressed metabolic enzyme, has recently been shown to enhance mtROS production and melanoma progression. However, how Arg-II enhances whether involved stimulation cancer cell proliferation migration remain unclear. Methods results Here, we show that ablation arg-ii suppresses growth, migration, nuclear deformation, DNA damage Vice versa,...
Aging is a predominant risk factor for cardiovascular diseases. There evidence demonstrating that senescent cells not only play significant role in organism aging but also contribute to the pathogenesis of diseases younger ages. Encouraged by recent findings elimination pharmacogenetic tools could slow down and even reverse animal models, senolytic drugs have been developed, translation results from basic research clinical settings has initiated. Because numerous studies literature show...
Abstract Elevated arginases including type‐I (Arg‐I) and type‐II isoenzyme (Arg‐II) are reported to play a role in aging, age‐associated organ inflammaging, fibrosis. A of arginase pulmonary aging underlying mechanisms not explored. Our present study shows increased Arg‐II levels lung female mice, which is detected bronchial ciliated epithelium, club cells, alveolar type 2 (AT2) pneumocytes, fibroblasts (but vascular endothelial smooth muscle cells). Similar cellular localization also...
The ureohydrolase, type-II arginase (Arg-II), is a mitochondrial enzyme metabolizing L-arginine into urea and L-ornithine highly expressed in renal proximal tubular cells (PTC) upregulated by ischemia. Recent studies reported contradictory results on the role of Arg-II injury. aim our study to investigate function epithelial cell damage under hypoxic conditions. Human line HK2 was cultured conditions for 12-48 h. Moreover, ex vivo experiments with isolated kidneys from wild-type (WT) genetic...
Aging is a predominant risk factor for heart disease. reveals low-grade chronic inflammation, cell apoptosis, cardiac fibrosis, and increased vulnerability to ischemic injury. The underlying molecular mechanisms responsible the aging phenotype its susceptibility injury are far from being fully understood. Although previous literature reports role of mitochondrial enzyme arginase-II (Arg-II) in development failure, contradictory results reported no systematic analysis cellular expression...
Increased protein phosphatase 1 (PP-1) activity has been found in end stage human heart failure. Although PP-1 extensively studied, a detailed understanding of its role the excitation-contraction coupling mechanism, normal and diseased hearts, remains elusive. The present study investigates functional effect on local Ca2+ release events ventricular cardiomyocytes, by using an activating peptide (PDP3) for stimulation endogenous protein. We report that acute de-phosphorylation may increase...
Hypoxia plays a crucial role in acute and chronic renal injury, which is attributable to tubular glomerular cell damage. Some studies provide evidence that hypoxia-dependent upregulation of the mitochondrial enzyme arginase type-II (Arg-II) cells promotes injury. It is, however, not known whether Arg-II also expressed cells, particularly podocytes under hypoxic conditions, contributing hypoxia-induced podocyte The effects hypoxia on human (AB8/13) cultures isolated kidneys from wild-type...
Hypoxia is an important risk for renal disease. The mitochondrial enzyme arginase-II (Arg-II) expressed and/or induced by hypoxia in proximal tubular epithelial cells (PTECs) and podocytes, leading to cellular damage. Because PTECs are vulnerable located proximity we examined the role of Arg-II crosstalk under hypoxic conditions with podocytes. A human PTEC cell line (HK2) a podocyte (AB8/13) were cultured. Arg-ii gene was ablated CRISPR/Case9 both types. HK2 exposed normoxia (21% O2) or (1%...
Abstract During exercise or stress, the sympathetic system stimulates cardiac contractility via β‐adrenergic receptor (β‐AR) activation, resulting in phosphorylation of ryanodine (RyR2). Three RyR2 sites have taken prominence excitation–contraction coupling: S2808 and S2030 are described as protein kinase A specific S2814 a Ca 2+ /calmodulin type‐2‐specific site. To examine contribution these phosphosites to signalling, we generated double knock‐in (DKI) mice which Ser2808 Ser2814 both been...
Aging is a predominant risk factor for heart disease. reveals low-grade chronic inflammation, cell apoptosis, cardiac fibrosis, and increased vulnerability to ischemic injury. The underlying molecular mechanisms responsible the aging phenotype its susceptibility injury are far from being fully understood. Although previous literature reports role of mitochondrial enzyme arginase-II (Arg-II) in development failure, contradictory results reported no systematic analysis cellular expression...
Aging is a predominant risk factor for heart disease. reveals low-grade chronic inflammation, cell apoptosis, cardiac fibrosis, and increased vulnerability to ischemic injury. The underlying molecular mechanisms responsible the aging phenotype its susceptibility injury are far from being fully understood. Although previous literature reports role of mitochondrial enzyme arginase-II (Arg-II) in development failure, contradictory results reported no systematic analysis cellular expression...
Abstract Background Aging-associated cardiac structural and functional alterations enhance susceptibility to ischemic injury. The full elucidation of the underlying molecular mechanisms remains far from complete. mitochondrial enzyme arginase-II (Arg-II) is implicated in injury aging. However, contradictory results have been reported no systemic analysis its cellular localization has performed. involvement Arg-II aging, as well manner which it participates, uncertain. Aim methods: This...
Age-associated sarcopenia decreases mobility and is promoted by cell senescence, inflammation, fibrosis. The mitochondrial enzyme arginase-II (Arg-II) plays a causal role in aging age-associated diseases. Therefore, we aim to explore the of Arg-II decline physical activity skeletal muscle mouse model. Young (4-6 months) old (20-24 wild-type (
One of the manifestations renal aging is podocyte dysfunction and loss, which are associated with proteinuria glomerulosclerosis. Studies show a male bias in glomerular chronic kidney diseases, underlying mechanisms remain obscure. Recent studies demonstrate role an age-associated increase arginase-II (Arg-II) proximal tubules both female mice. However, it unclear whether Arg-II also involved glomeruli. The current study investigates sex-specific elevation podocytes increased albuminuria....