A5066508291- Autophagy in Disease and Therapy
- Genetic and Kidney Cyst Diseases
- Calcium signaling and nucleotide metabolism
- Cannabis and Cannabinoid Research
- Biomedical Research and Pathophysiology
- Endoplasmic Reticulum Stress and Disease
- Renal and related cancers
- Mitochondrial Function and Pathology
- Apelin-related biomedical research
- Cardiovascular, Neuropeptides, and Oxidative Stress Research
- Genetic Syndromes and Imprinting
- Advanced Glycation End Products research
- Metabolism and Genetic Disorders
- Cardiac Ischemia and Reperfusion
- Sirtuins and Resveratrol in Medicine
- Organ Transplantation Techniques and Outcomes
- Adenosine and Purinergic Signaling
- Renal Diseases and Glomerulopathies
- Parkinson's Disease Mechanisms and Treatments
- Neuroscience and Neuropharmacology Research
- Plant responses to water stress
- Pancreatic function and diabetes
- Acute Kidney Injury Research
- RNA Interference and Gene Delivery
- Hormonal Regulation and Hypertension
KU Leuven
2013-2024
VIB-KU Leuven Center for Microbiology
2024
VIB-KU Leuven Center for Brain & Disease Research
2017-2023
VIB-KU Leuven Center for Cancer Biology
2011-2016
Universitair Ziekenhuis Leuven
2015
Catholic University of America
2014
Toxicologie, Pharmacologie et Signalisation Cellulaire
2011-2013
Institut de Biologie Moléculaire et Cellulaire
2011
Autophagy is an intracellular degradation process responsible for the delivery of cellular material to lysosomes. One key mechanisms control autophagy modulation interaction between autophagic protein Beclin 1 and members anti-apoptotic Bcl-2 family (e.g., Bcl-2, Bcl-XL Mcl-1). This binding regulated by a variety proteins compounds that are able enhance or inhibit Bcl-2/Beclin in order repress activate autophagy, respectively. In this review we will focus on discuss its characteristics,...
The role of intracellular Ca2+ signaling in starvation-induced autophagy remains unclear. Here, we examined dynamics during and the underlying molecular mechanisms. Tightly correlating with stimulation, observed a remodeling signalosome. First, short periods starvation (1 to 3 h) caused prominent increase ER Ca2+-store content enhanced agonist-induced release. mechanism involved upregulation intralumenal Ca2+-binding proteins, calreticulin Grp78/BiP, which increased Ca2+-buffering capacity...
Abstract Superparamagnetic iron oxide nanoparticles (SPIONs) have mainly been used as cellular carriers for genes and therapeutic products, while their use in subcellular organelle isolation remains underexploited. We engineered SPIONs targeting distinct compartments. Dimercaptosuccinic acid-coated are internalized accumulate late endosomes/lysosomes, aminolipid-SPIONs reside at the plasma membrane. These features allowed us to establish standardized magnetic procedures these membrane...
Autophagy is a lysosomal degradation pathway important for cellular homeostasis and survival. Inhibition of the mammalian target rapamycin (mTOR) best known trigger autophagy stimulation. In addition, intracellular Ca2+ regulates autophagy, but its exact role remains ambiguous. Here, we report that mTOR inhibitor rapamycin, while enhancing also remodeled Ca2+-signaling machinery. These alterations include a) an increase in endoplasmic-reticulum (ER) Ca2+-store content, b) decrease ER...
The tight interplay between endoplasmic-reticulum-(ER-) and mitochondria-mediated Ca 2+ signaling is a key determinant of cellular health fate through the control apoptosis autophagy. Proteins that prevent or promote autophagy can affect intracellular dynamics homeostasis binding modulation -release -uptake mechanisms. During aging, oxidative stress becomes an additional factor affects ER mitochondrial function thus their role in signaling. Importantly, dysfunction sustained damage are...
Autophagy is an important cell-biological process responsible for the disposal of long-lived proteins, protein aggregates, defective organelles and intracellular pathogens. It activated in response to cellular stress plays a role development, cell differentiation, ageing. Moreover, it has been shown be involved different pathologies, including cancer neurodegenerative diseases. long standing issue whether how Ca2+ ion its regulation. The inositol 1,4,5-trisphosphate receptor, main...
Stromal interaction molecules (STIM) were identified as the endoplasmic-reticulum (ER) Ca2+ sensor controlling store-operated entry (SOCE) and Ca2+-release-activated (CRAC) channels in non-excitable cells. STIM proteins target Orai1-3, tetrameric Ca2+-permeable plasma membrane. Structure-function analysis revealed molecular determinants key steps activation process of Orai by STIM. Recently, STIM1 was found to be expressed at high levels skeletal muscle function properties. Novel targets...
Introduction The farnesoid X receptor (FXR) is abundantly expressed in the ileum, where it exerts an enteroprotective role as a key regulator of intestinal innate immunity and homeostasis, shown pre-clinical models inflammatory bowel disease. Since ischemia reperfusion injury (IRI) characterized by hyperpermeability, bacterial translocation inflammation, we aimed to investigate, for first time, if FXR-agonist obeticholic acid (OCA) could attenuate injury. Material Methods In validated rat...
Renal ischemia-reperfusion (IR) injury leading to cell death is a major cause of acute kidney injury, contributing morbidity and mortality. Autophagy counteracts by removing damaged macromolecules organelles, making it an interesting anchor point for treatment strategies. However, autophagy also suggested enhance when the ischemic burden too strong. To investigate whether role depends on severity stress, we analyzed dynamics apoptosis in IR rat model with mild (45 min) or severe (60 renal...
Functional intracellular Ca(2+) signaling is essential for the upregulation of canonical mTOR-controlled autophagy pathway triggered by rapamycin or nutrient deprivation. Moreover, modifications in Ca(2+)-signaling machinery coincide with stimulation. This results enhanced driving process. Yet, mechanisms upstream (the players causing changes signaling) and downstream targets altered signals) this Ca(2+)-dependent remain elusive. Here, we speculate about these based on our current knowledge.
Apolipoprotein L1 (APOL1) high-risk genotypes (HRG), G1 and G2, increase the risk of various non-diabetic kidney diseases in African population. To date, precise mechanisms by which APOL1 variants induce injury on podocytes other cells remain unclear. Trying to unravel these mechanisms, most studies have used animal or cell models created gene editing. We developed characterised conditionally immortalised human podocyte lines derived from urine a donor carrying HRG G2/G2. Following induction...
Autosomal dominant polycystic kidney disease (ADPKD) is mainly caused by deficiency of polycystin-1 (PC1) or polycystin-2 (PC2). Altered autophagy has recently been implicated in ADPKD progression, but its exact regulation PC1 and PC2 remains unclear. We therefore investigated cell death survival during nutritional stress mouse inner medullary collecting duct cells (mIMCDs), either wild-type (WT) lacking (PC1KO) (PC2KO), human urine-derived proximal tubular epithelial (PTEC) from early-stage...