Martina Zandl‐Lang

Medical University of Graz

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Ute Panzenboeck

Medical University of Graz

Alexandra Kober

University of Applied Sciences Potsdam

Elham Fanaee‐Danesh

Medical University of Graz

Nicole Maria Albrecher

Medical University of Graz

Chaitanya Chakravarthi Gali

Medicover

Anil Paul Chirackal Manavalan

Central European Institute of Technology

Barbara Plecko

Medical University of Graz

Dagmar Kratky

Medical University of Graz

Jyotsna B. Pippal

Medical University of Graz

Harald Köfeler

Medical University of Graz

Cooperative Institutions

Medical University of Graz

University of Graz

BioTechMed-Graz

Graz University of Technology

Weatherford College

Nawi Graz

University of Zurich

Rudjer Boskovic Institute

Institute of Biochemistry

University Children's Hospital Zurich

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Regulatory effects of simvastatin and apoJ on APP processing and amyloid-β clearance in blood-brain barrier endothelial cells

Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids (2017)

Martina Zandl‐Lang Elham Fanaee‐Danesh Yidan Sun Nicole Maria Albrecher Chaitanya Chakravarthi Gali

LRP1

Apolipoprotein E

10.1016/j.bbalip.2017.09.008

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Citations (56)

LIVER-X RECEPTOR AGONISTS MODULATE HDL AND AMYLOID-BETA METABOLISM IN BRAIN CAPILLARY ENDOTHELIAL CELLS FORMING THE BLOOD-BRAIN BARRIER

WOS (2014)

Ute Panzenboeck Anil Paul Chirackal Manavalan Alexandra Kober Cornelia Schweinzer Jari Metso

BETA (programming language)

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5-HT3A receptor in Salipro (apo, C5 symmetric)

Y. Zhang Patricia M. Dijkman Rongfeng Zou Martina Zandl‐Lang Ricardo Sánchez

10.2210/pdb6y59/pdb

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Regulation of the yeast triacylglycerol lipases Tgl4p and Tgl5p by the presence/absence of nonpolar lipids

Molecular Biology of the Cell (2016)

Isabella Klein Lisa Klug Claudia Schmidt Martina Zandl‐Lang Martina Korber

Tgl3p, Tgl4p, and Tgl5p are the major triacylglycerol lipases of the yeast Saccharomyces cerevisiae Recently we demonstrated that properties of Tgl3p are regulated by the formation of nonpolar lipids. The present study extends these investigations to the two other yeast triacylglycerol lipases, Tgl4p and Tgl5p. We show that Tgl4p and Tgl5p, which are localized to lipid droplets in wild type, are partially retained in the endoplasmic reticulum in cells lacking triacylglycerols and localize exclusively to the endoplasmic reticulum in a mutant devoid of lipid droplets. In cells lacking steryl esters, the subcellular distribution of Tgl4p and Tgl5p is unaffected, but Tgl5p becomes unstable, whereas the stability of Tgl4p increases. In cells lacking nonpolar lipids, Tgl4p and Tgl5p lose their lipolytic activity but retain their side activity as lysophospholipid acyltransferases. To investigate the regulatory network of yeast triacylglycerol lipases in more detail, we also examined properties of Tgl3p, Tgl4p, and Tgl5p, respectively, in the absence of the other lipases. Surprisingly, lack of two lipases did not affect expression, localization, and stability of the remaining Tgl protein. These results suggest that Tgl3p, Tgl4p, and Tgl5p, although they exhibit similar functions, act as independent entities.

10.1091/mbc.e15-09-0633

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The regulatory network of yeast triacylglycerol lipases

Günther Daum Claudia Schmidt Martina Zandl‐Lang Lisa Klug Isabella Klein

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Lipidomics in Rett Syndrome Patients

Zenodo (CERN European Organization for Nuclear Research) (2022)

Martina Zandl‐Lang

Lipidomics analysis of CSF and plasma samples obtained from Rett syndrome (RS) patients and controls using UHPLC-MS/MS. Raw data (Panasonic raw image) obtained from analysis in positive and negative ionisation mode. Processed results files from each sample are shown in separate excel files. Enclosed meta file provides sample information.

Rett Syndrome

10.5281/zenodo.5947668

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Tracing the lipidome in inborn errors of metabolism

Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids (2024)

Martina Zandl‐Lang

Inborn errors of metabolism (IEM) represent a heterogeneous group of more than 1800 rare disorders, many of which are causing significant childhood morbidity and mortality. More than 100 IEM are linked to dyslipidaemia, but yet our knowledge in connecting genetic information with lipidomic data is limited. Stable isotope tracing studies of the lipid metabolism (STL) provide insights on the dynamic of cellular lipid processes and could thereby facilitate the delineation of underlying metabolic (patho)mechanisms. This mini-review focuses on principles as well as technical limitations of STL and describes potential clinical applications by discussing recently published STL focusing on IEM.

Tracing

Lipidome

10.1016/j.bbalip.2024.159491

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Citations (1)

P1‐111: PHOSPHOLIPID TRANSFER PROTEIN IS EXPRESSED AND INVOLVED IN HDL BIOGENESIS AND REMODELING AT THE BLOOD‐BRAIN BARRIER

Alzheimer s & Dementia (2014)

Anil Manavalan Paul Elham Fanaee‐Danesh Alexandra Kober Martina Zandl‐Lang Jyotsna B. Pippal

High plasma high-density lipoproteins (HDL) protect against neurodegenerative disease. However, the underlying mechanisms are largely unexplored. Phospholipid transfer protein (PLTP) is a key protein involved in plasma HDL remodeling and is thought to influence pathogenesis of Alzheimer's disease. We reported earlier that liver-X receptor (LXR) activation promotes cellular cholesterol efflux and formation of HDL-like particles in an in vitro model of the blood-brain barrier (BBB) consisting of porcine brain capillary endothelial cells. We here hypothesized that BCEC may express PLTP which may be involved in HDL metabolism in the brain. Immunohisto/cytochemical staining of porcine brain and cultured primary pBCEC.mRNA expression levels were determined by real-time PCR.PL transfer activity in pBCEC supernatants, cell lysates and in transwell supernatants was determined by radiometric assay. PLTP is expressed in cerebrovascular endothelial cells PLTP expression and activity are up-regulated by LXR activation and in a polarized manner PLTP-mediated modification increases the cholesterol removal capacity of HDL 3 LXR activation up-regulates PLTP activity in vivo Endogenous PLTP remodels HDL and pre β-HDL formation is enhanced by LXR agonist PLTP silencing disrupts the biogenesis of HDL particles Phospholipid transfer protein is expressed in cerebrovascular endothelial cells and involved in HDL biogenesis and remodeling at the blood brain barrier.

Phospholipid transfer protein

Liver X receptor

10.1016/j.jalz.2014.05.348

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Lipidomics—Paving the Road towards Better Insight and Precision Medicine in Rare Metabolic Diseases

International Journal of Molecular Sciences (2023)

Martina Zandl‐Lang Barbara Plecko Harald Köfeler

Even though the application of Next-Generation Sequencing (NGS) has significantly facilitated the identification of disease-associated mutations, the diagnostic rate of rare diseases is still below 50%. This causes a diagnostic odyssey and prevents specific treatment, as well as genetic counseling for further family planning. Increasing the diagnostic rate and reducing the time to diagnosis in children with unclear disease are crucial for a better patient outcome and improvement of quality of life. In many cases, NGS reveals variants of unknown significance (VUS) that need further investigations. The delineation of novel (lipid) biomarkers is not only crucial to prove the pathogenicity of VUS, but provides surrogate parameters for the monitoring of disease progression and therapeutic interventions. Lipids are essential organic compounds in living organisms, serving as building blocks for cellular membranes, energy storage and signaling molecules. Among other disorders, an imbalance in lipid homeostasis can lead to chronic inflammation, vascular dysfunction and neurodegenerative diseases. Therefore, analyzing lipids in biological samples provides great insight into the underlying functional role of lipids in healthy and disease statuses. The method of choice for lipid analysis and/or huge assemblies of lipids (=lipidome) is mass spectrometry due to its high sensitivity and specificity. Due to the inherent chemical complexity of the lipidome and the consequent challenges associated with analyzing it, progress in the field of lipidomics has lagged behind other omics disciplines. However, compared to the previous decade, the output of publications on lipidomics has increased more than 17-fold within the last decade and has, therefore, become one of the fastest-growing research fields. Combining multiple omics approaches will provide a unique and efficient tool for determining pathogenicity of VUS at the functional level, and thereby identifying rare, as well as novel, genetic disorders by molecular techniques and biochemical analyses.

Lipidome

Omics

10.3390/ijms24021709

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Citations (11)

P1‐058: SIMVASTATIN INFLUENCES APOJ AND AMYLOID‐BETA METABOLISM IN CEREBROVASCULAR ENDOTHELIAL CELLS

Alzheimer s & Dementia (2014)

Martina Zandl‐Lang Jyotsna B. Pippal Elham Danesh Alexandra Kober Cornelia Schweinzer

The overproduction and accumulation of amyloid-beta (Aβ) plays a crucial role in the pathogenesis of Alzheimer's Disease (AD). Aβ accumulation in cerebral capillaries can lead to cerebral amyloid angiopathy, indicating a thus far underestimated role of the blood-brain barrier (BBB) in the pathogenesis of the disease. In addition, it has become increasingly evident that apoJ, also known as clusterin, is involved in cholesterol/lipid trafficking in the brain. Previous studies revealed an increase of apoJ expression in AD. ApoJ can bind to Aβ peptides, prevents their fibrillization, and thereby enhances endocytosis by glial cells. Although evidence exists for a close connection between peripheral and cerebral apolipoprotein-, cholesterol- and amyloid precursor protein (APP)/Aβ metabolism, information about the interconnecting mechanisms occurring in or mediated by brain capillary endothelial cells (BCEC) is lacking. Our central aim is to define the involvement of apoJ in cholesterol, and APP/ Aβ metabolism at the BBB. Primary porcine (p)BCEC were incubated with modulators of cellular cholesterol metabolism, i.e. the endogenous LXR agonists 24(S)OH-cholesterol and 27OH-cholesterol, the synthetic LXR ligand TO901317, cholesterol, and the HMGCo-A reductase inhibitor simvastatin. Protein and mRNA expression levels of apoJ, APP/Aβ and enzymes of the amyloid cascade were part of the examinations. Furthermore, to obtain polarized secretion of apoJ and APP products to the basolateral (mimicking the brain-parenchymal side of the BBB) and apical compartments (mimicking the blood-side of the BBB), pBCEC are cultured on multiwell transwell filters in the absence or presence of modulators of cholesterol metabolism. Real-time PCR and immunoblotting analyses suggest a higher expression of both apoJ and APP mRNA and protein, respectively, in response to simvastatin treatment. Results obtained during transwell studies suggest a release of apoJ primarily to the basolateral as compared to the apical compartment, which is altered by modulating cellular cholesterol metabolism. ApoJ synthesis and secretion towards the basolateral compartment of the BBB may suggest a beneficial role of apoJ in APP/Aβ metabolism. Since APP processing and production of Aβ is linked to cholesterol homeostasis, future experiments are aiming to elucidate the role of apoJ in APP/Aβ metabolism at the BBB in vitro (and in vivo).

Pathogenesis

Clusterin

Amyloid beta

10.1016/j.jalz.2014.05.294

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