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Biology subjects

Sarparast, M.

Publications and source records attributed to Sarparast, M..

4 recordsLinked to original sources

A Robust Chemical-free Platform for Age-Synchronized Caenorhabditis elegans Populations Maintenance for High-Throughput Screening in Aging Studies

Caenorhabditis elegans (C. elegans) is a well-established model for investigating the mechanisms of aging and age-related disorders like neurodegeneration. However, maintaining age-synchronized populations of C. elegans for aging studies without genetic or pharmacological interventions presents significant challenges, given their high reproductive rate: each nematode produces over 300 progeny. The traditional method for maintaining an age-synchronized population for multi-day studies without interventions is labor-intensive and low-throughput, hindering research on aging mechanisms and the identification of novel interventions for aging. To address these limitations, a novel, robust method was developed to sustain age-synchronized populations in a 96-well plate liquid culture format for up to 12 days without custom-made apparatuses. The robustness of this method was substantially improved by optimizing the surface composition of the multi-well plate and disposables, refining culture parameters, including life stage, medium composition, and bacterial food concentration. To facilitate unbiased phenotype assessment throughout the lifespan, we used a Wmicrotracker ONE reader to monitor worm movement and viability in a multi-well plate. The overall fitness decline with aging using our method is comparable to that of worms maintained on solid agar. Lastly, using transgenic C. elegans carrying tauopathy, we demonstrated the ability of applying our optimized platform for high-throughput screening with a Z-factor of 0.7. Our novel method simplifies age-synchronized population maintenance, enhances progeny separation, and reduces costs, enabling high-throughput screening of compounds and RNAi libraries. These advancements greatly enhance the versatility of C. elegans as a model organism, offering a scalable platform for genetic and compound screening and for comprehensive investigations into drug discovery and disease mechanisms.

pharmacology and toxicology↗

Quantitative Profiling Method for Oxylipins in Neurodegenerative Diseases by Liquid Chromatography Coupled with Tandem Mass Spectrometry

Aging is one of the major risk factors for many chronic diseases, including diabetes, neuropathy, hypertension, cancer, and neurodegenerative diseases. However, the mechanism behind aging and how aging affects a variety of disease progression remains unknown. Recent research demonstrated the cytochrome P450 (CYP)-epoxide hydrolase (EH) metabolites of polyunsaturated fatty acids (PUFAs) play a critical role in the abovementioned age-associated diseases. Therefore, aging could affect the abovementioned chronic diseases by modulating CYP-EH PUFA metabolism. Unfortunately, investigating how aging affects CYP-EH metabolism in human and mammalian models poses significant challenges. In this regard, we will use C. elegans as a model organism to investigate the aging effects on CYP-EH metabolism of PUFA, owing to its long history of being used to study aging and its associated benefits of conducting aging research. This project will develop analytical tools to measure the endogenous levels of CYP-EH PUFA metabolites in C. elegans using state-of-the-art ultra-performance liquid chromatography coupled with tandem mass spectrometry (UPLC-MS/MS). These metabolites are very potent but present in low abundance. The dramatic increase in sensitivity in UPLC-MS/MS allows us to monitor these metabolites over the lifespan of C. elegans with minimum samples. Our results show that C. elegans produces similar CYP PUFA metabolites to mammals and humans using our SPE-UPLC-MS/MS method. We will also show that our method successfully determined the CYP-EH PUFA metabolites profile changes induced by the inhibition of C. elegans EH. The method developed from this project will significantly improve our understanding of the role of dietary PUFAs and associated metabolism on aging and neurodegeneration and will uncover new mechanisms of how aging affects neurodegeneration through the modulation of PUFA metabolic pathways. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=121 SRC="FIGDIR/small/560544v1_ufig1.gif" ALT="Figure 1"> View larger version (22K): org.highwire.dtl.DTLVardef@415035org.highwire.dtl.DTLVardef@1f8d81eorg.highwire.dtl.DTLVardef@34a9f8org.highwire.dtl.DTLVardef@182de04_HPS_FORMAT_FIGEXP M_FIG C_FIG

physiology↗

Cytochrome P450 and Epoxide Hydrolase Metabolites in Aβ and tau-induced Neurodegeneration: Insights from Caenorhabditis elegans

This study aims to uncover potent cytochrome P450 (CYP) and epoxide hydrolase (EH) metabolites implicated in A{beta} and/or tau-induced neurodegeneration, independent of neuroinflammation, by utilizing Caenorhabditis elegans (C. elegans) as a model organism. Our research reveals that A{beta} and/or tau expression in C. elegans disrupts the oxylipin profile, and epoxide hydrolase inhibition alleviates the ensuing neurodegeneration, likely through elevating the epoxy-to-hydroxy ratio of various CYP-EH metabolites. In addition, our results indicated that the A{beta} and tau likely affect the CYP-EH metabolism of PUFA through different mechanism. These findings emphasize the intriguing relationship between lipid metabolites and neurodegenerations, in particular, those linked to A{beta} and/or tau aggregation. Furthermore, our investigation sheds light on the crucial and captivating role of CYP PUFA metabolites in C. elegans physiology, opening up possibilities for broader implications in mammalian and human contexts. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=92 SRC="FIGDIR/small/560527v1_ufig1.gif" ALT="Figure 1"> View larger version (22K): org.highwire.dtl.DTLVardef@8fd3fdorg.highwire.dtl.DTLVardef@a6c4e1org.highwire.dtl.DTLVardef@c7a5a7org.highwire.dtl.DTLVardef@14c8ce2_HPS_FORMAT_FIGEXP M_FIG C_FIG

neuroscience↗

Dihydroxy-Metabolites of Dihomo-gamma-linolenic Acid Drive Ferroptosis- Mediated Neurodegeneration

Even after decades of research, the mechanism of neurodegeneration remains understudied, hindering the discovery of effective treatments for neurodegenerative diseases. Recent reports suggest that ferroptosis could be a novel therapeutic target for neurodegenerative diseases. While polyunsaturated fatty acid (PUFA) plays an important role in neurodegeneration and ferroptosis, how PUFAs may trigger these processes remains largely unknown. PUFA metabolites from cytochrome P450 and epoxide hydrolase metabolic pathways may modulate neurodegeneration. Here, we test the hypothesis that specific PUFAs regulate neurodegeneration through the action of their downstream metabolites by affecting ferroptosis. We find that the PUFA, dihomo gamma linolenic acid (DGLA), specifically induces ferroptosis-mediated neurodegeneration in dopaminergic neurons. Using synthetic chemical probes, targeted metabolomics, and genetic mutants, we show that DGLA triggers neurodegeneration upon conversion to dihydroxyeicosadienoic acid through the action of CYP-EH, representing a new class of lipid metabolite that induces neurodegeneration via ferroptosis.

neuroscience↗