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The MT1G gene in LUHMES Neurons is a Sensitive Biomarker of Neurotoxicity

ABSTRACT: The MT1G gene in LUHMES Neurons is a Sensitive Biomarker of Neurotoxicity

PROVIDER: PRJNA630786 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11719900_1.fastq.gz	Fastqsanger.gz
	SRR11719900_2.fastq.gz	Fastqsanger.gz
	SRR11719901_1.fastq.gz	Fastqsanger.gz
	SRR11719901_2.fastq.gz	Fastqsanger.gz
	SRR11719902_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

The MT1G gene in LUHMES Neurons is a Sensitive Biomarker of Neurotoxicity

Project description:Identification of toxicants that underlie neurological diseases is a neglected area awaiting a valid strategy to identify such toxicants. We sought biomarkers that respond to known neurotoxicants in LUHMES immortalized neurons and evaluated these biomarkers for use in screening libraries of environmental toxicants. LUHMES immortalized human dopaminergic neurons were surveyed by RNA sequencing following challenge with Parkinsonian toxicants rotenone, 6-hydroxydopamine, MPP+, and ziram (zinc dimethyldithiocarbamate; Zn2+DDC2), as well as additional toxicants paraquat, MS275, and methylmercury. The metallothionein gene MT1G was the most dynamic gene expression response to all seven toxicants. Multiple toxicants also increased transcripts for SLC30A1 and SLC30A2 zinc secretion transporters, the SLC7A11 xCT cystine/glutamate antiporter important for glutathione synthesis, DNA damage Inducible Transcript 3 (DDIT3), and secreted growth factors FIBIN and CXCL12, whereas several toxicants decreased expression of the Apelin growth factor (APLN). These biomarker genes showed advantages in sensitivity by responding to many toxicants at sub-cytotoxic concentrations. Since several of these biomarker genes and prior neurological disease studies implicated disruption of metal distribution, we tested metal chelator thiram (dimethyldithiocarbamate, DDC), Zn2+DDC2, and several other metals and metal chelates for cytoxicity and induction of MT1G expression. Metals and chelators that caused dynamic increases in MT1G expression caused cytotoxicity, whereas Ni2+DDC2 caused MT1G increase, but no cytotoxicity. These results bolster prior work suggesting that neurons are characteristically sensitive to depletion of glutathione or to disruption of cellular metal distribution and provide biomarkers to search for such neurotoxicants in chemical libraries.

2020-08-11 | GSE150005 | GEO

The MT1G Gene in LUHMES Neurons Is a Sensitive Biomarker of Neurotoxicity.

Project description:Identification of toxicants that underlie neurological diseases is a neglected area awaiting a valid strategy to identify such toxicants. We sought biomarkers that respond to known neurotoxicants in LUHMES immortalized neurons and evaluated these biomarkers for use in screening libraries of environmental toxicants. LUHMES immortalized human dopaminergic neurons were surveyed by RNA sequencing following challenge with parkinsonian toxicants rotenone, 6-hydroxydopamine, MPP+, and ziram (zinc dimethyldithiocarbamate; Zn2+DDC2), as well as additional toxicants paraquat, MS275, and methylmercury. The metallothionein gene MT1G was the most dynamic gene expression response to all seven toxicants. Multiple toxicants also increased transcripts for SLC30A1 and SLC30A2 zinc secretion transporters, the SLC7A11 xCT cystine/glutamate antiporter important for glutathione synthesis, DNA damage inducible transcript 3 (DDIT3), and secreted growth factors FIBIN and CXCL12, whereas several toxicants decreased expression of the apelin growth factor (APLN). These biomarker genes revealed stress responses to many toxicants at sub-cytotoxic concentrations. Since several of these biomarker genes and prior neurological disease studies implicated disruption of metal distribution, we tested metal chelator thiram (dimethyldithiocarbamate, DDC), ziram, and several other metals and metal chelates for cytotoxicity and induction of MT1G expression. Metals and chelators that caused dynamic increases in MT1G expression also caused cytotoxicity, except Ni2+DDC2 induced MT1G at 5 μM, but lacked cytotoxicity up to 100 μM. These results bolster prior work suggesting that neurons are characteristically sensitive to depletion of glutathione or to disruption of cellular metal distribution and provide biomarkers to search for such neurotoxicants in chemical libraries.

| S-EPMC7765730 | biostudies-literature

RNA-seq of CSMD1 enhancer CRISPRi in LUHMES cells and differentiated neurons

Project description:we performed lentiviral CRISPR interference (CRISPRi) by recruiting dCas9 fused with the KRAB domain to the CSMD1 enhancer (fam3) in the neuronal precursor cell line – Lund human mesencephalic (LUHMES). Given that the expression of CSMD1 was not detectable in LUHMES cells we differentiated these cells into neurons. Differentiated neurons with CRISPRi of CSMD1 enhancer showed significantly higher expression of CSMD1 than control.

2022-06-30 | E-MTAB-8027 | biostudies-arrayexpress

Neuronal differentiation of LUHMES cells is accompanied by substantial changes of the proteome

Project description:To study mechanisms of neurodegenerative diseases, neuronal cell lines are important model systems and are often differentiated into postmitotic neuron-like cells to resemble more closely primary neurons obtained from brains. One such cell line is the Lund Human Mesencephalic (LUHMES) cell line which can be differentiated into dopamine-like neurons and is frequently used to study mechanisms of Parkinson’s disease (PD) and neurotoxicity. Neuronal differentiation of LUHMES cells is commonly verified by measurement of selected neuronal markers, but little is known about proteome-wide protein abundance changes during differentiation. Using mass spectrometry and label-free quantification (LFQ) we compared the proteome of differentiated and undifferentiated LUHMES cells as well as of cultured primary murine midbrain neurons, which are mainly dopaminergic. Neuronal differentiation induced substantial changes of the LUHMES cell proteome (18.4% reveal protein abundance changes of more than 4-fold), with proliferation-related proteins (e.g. MCMs) being strongly down-regulated and neuronal and dopaminergic proteins being up to 1000-fold upregulated, such as L1CAM and SNCA. Several of these proteins, including MAPT and SYN1, may be useful new markers to experimentally validate neuronal differentiation of cultured LUHMES cells. Primary midbrain neurons were more closely related to differentiated than to undifferentiated LUHMES cells with respect to the abundance of proteins related to neurodegeneration or to genetic forms of PD. In summary, our comparative proteomic analysis demonstrates that differentiated LUHMES cells are a suitable model for studies on PD and neurodegeneration and provides a resource of the proteome-wide changes during neuronal differentiation.

2020-09-24 | PXD020044 | Pride

Study of MeCP2 in LUHMES-derived neurons

Project description:Study of MeCP2 in LUHMES-derived neurons

| PRJNA517116 | ENA

Transcriptome and proteome analysis in LUHMES cells overexpressing alpha-synculein

Project description:LUHMES cells share many characteritics with human dopamingeric neurons in the substantia nigra, the cells whose demise is responsible for the motor symptoms in Parkinson’s disease (PD). LUHMES cells can therefore be used bona fide as a model to study pathophysiological processes involved in PD. Previously, we showed that LUHMES cell degenerate after six days upon overexpression of wild type alpha-synuclein. In the present study we performed a transcriptome and proteome expression analysis in alpha-synuclein-overexpressing cells and GFP-expressing control cells in order to identify genes and proteins that are differentially regulated upon overexpression of alpha-synuclein. The analysis was performed four days after the initiation of alpha-synuclein or GFP overexpression, before the cells died in order to identify processes that preceded cell death.

2022-05-19 | PXD028322 | Pride

RNA-seq of CSMD1 enhancer CRISPRi in LUHMES cells and differentiated neurons

Project description:RNA-seq of CSMD1 enhancer CRISPRi in LUHMES cells and differentiated neurons

| PRJEB32901 | ENA

Transcriptome and proteome analysis in LUHMES cells overexpressing alpha-synuclein

Project description:Differential transcriptome analysis in LUHMES cells overexpressing human wild-type alpha-synuclein or GFP

2022-03-31 | GSE191302 | GEO

Capture Hi-C (HiCap) experiments performed on LUHMES cell line differentiated in three (D3) and six days (D6). We fragmented the genome using DpnII. HiCap experiments at each time point (D1, D3 and D6) are performed in two replicates

Project description:LUHMES cells are non-tumorigenic model of human dopaminergic neurons. Their physiology and phenotypic changes upon differentiation can provide clues into the pathology of neurological diseases such as dyslexia, autism, schizophrenia.

2024-01-14 | E-MTAB-13665 | biostudies-arrayexpress

Expression data from Lund Human Mesencephalic cells (LUHMES) exposed to acute and persistent oxidative DNA damage

Project description:Oxidative DNA damage in neurons activates a DNA damage response (DDR) to promote repair. Under a chronic oxidative environment these processes may be altered and promote accumulation of unrepaired DNA damage and continued activation of a DDR, leading to apoptosis or senescence activation. Accumulation of oxidative DNA damage are features of brain ageing and neurodegeneration but the effects of persistent DNA damage in neurons are not well characterised. We developed a model of persistent oxidative DNA damage in human neurons in vitro (LUHMES) by exposing them to a sub-lethal concentration of hydrogen peroxide (H2O2) following a "single stress" and “double stress” protocols. We characterised the neuronal transcriptome under these circumstances using microarray analysis.

2023-11-04 | GSE160841 | GEO

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