#METABOLOMICS WORKBENCH mChu_20240710_120031 DATATRACK_ID:4996 STUDY_ID:ST003352 ANALYSIS_ID:AN005493 PROJECT_ID:PR001855
VERSION             	1
CREATED_ON             	July 17, 2024, 11:19 am
#PROJECT
PR:PROJECT_TITLE                 	Integrated multi-omics reveals mTOR-LPL-driven dysregulated lipid metabolism
PR:PROJECT_TITLE                 	induces neuronal hyperexcitability in human microglia of tuberous sclerosis
PR:PROJECT_TITLE                 	complex
PR:PROJECT_SUMMARY               	Tuberous sclerosis complex (TSC) is an autosomal dominant genetic disorder
PR:PROJECT_SUMMARY               	caused by mutations in either TSC1 or TSC2. There's evidence suggests a
PR:PROJECT_SUMMARY               	connection between microglia activation and epilepsy as well as cognitive
PR:PROJECT_SUMMARY               	impairment in TSC patients. However, how the causal variants of TSC1/2 genes
PR:PROJECT_SUMMARY               	identified in TSC patients affect human microglia and how they contribute to the
PR:PROJECT_SUMMARY               	neurological manifestations remains unclear. This project is focus on this
PR:PROJECT_SUMMARY               	problem using human microglia generated from induced pluripotent stem cells
PR:PROJECT_SUMMARY               	(iPSCs) derived from a TSC patient.
PR:INSTITUTE                     	Stjude children research hospital
PR:LAST_NAME                     	Chu
PR:FIRST_NAME                    	Mengqi
PR:ADDRESS                       	262 Danny Tomas Place, Memphis, Tennessee, 38104, USA
PR:EMAIL                         	Mengqi.Chu@stjude.org
PR:PHONE                         	901-603-2366
#STUDY
ST:STUDY_TITLE                   	Untargeted lipidomics profiling of LPL-overexpression and LPL-knockdown
ST:STUDY_TITLE                   	microglia
ST:STUDY_SUMMARY                 	In this study, human microglia from induced pluripotent stem cells (iPSCs)
ST:STUDY_SUMMARY                 	derived from a TSC patient cohort were generated. Upregulated
ST:STUDY_SUMMARY                 	glycerophosphocholines and fatty acyls were found in TSC microglia, resulting in
ST:STUDY_SUMMARY                 	increased phagocytosis and inflammation. Strikingly, the dysregulated lipid
ST:STUDY_SUMMARY                 	metabolism in TSC microglia is driven by hyper-activation of mTOR-lipoprotein
ST:STUDY_SUMMARY                 	lipase (LPL) pathway. Furthermore, cellular and electrophysiological assessments
ST:STUDY_SUMMARY                 	of neuron/microglia co-cultures revealed that TSC microglia directly affect
ST:STUDY_SUMMARY                 	neuronal development and excitability as well as neuronal network activity,
ST:STUDY_SUMMARY                 	which could be largely ameliorated by mTOR/LPL inhibition. Through integrated
ST:STUDY_SUMMARY                 	multi-omics analysis, levels of glycerophosphocholines were found increased in
ST:STUDY_SUMMARY                 	the microglia of humans with tuberous sclerosis complex. To determine whether
ST:STUDY_SUMMARY                 	glycerophosphocholines are regulated by the LPL gene, we performed experiments
ST:STUDY_SUMMARY                 	with LPL overexpression in microglia and LPL knockdown in microglia.
ST:INSTITUTE                     	Stjude children research hospital
ST:LAST_NAME                     	Chu
ST:FIRST_NAME                    	Mengqi
ST:ADDRESS                       	262 Danny Tomas Place, Memphis, Tennessee, 38104, USA
ST:EMAIL                         	Mengqi.Chu@stjude.org
ST:PHONE                         	901-603-2366
#SUBJECT
SU:SUBJECT_TYPE                  	Cultured cells
SU:SUBJECT_SPECIES               	Homo sapiens
SU:TAXONOMY_ID                   	9606
#SUBJECT_SAMPLE_FACTORS:         	SUBJECT(optional)[tab]SAMPLE[tab]FACTORS(NAME:VALUE pairs separated by |)[tab]Raw file names and additional sample data
SUBJECT_SAMPLE_FACTORS           	-	426_1	Genotype:WT | Treatment:Control for Overexpression | Sample source:iPSC	RAW_FILE_NAME(Raw file name)=426_1.mzXML
SUBJECT_SAMPLE_FACTORS           	-	426_2	Genotype:WT | Treatment:Control for Overexpression | Sample source:iPSC	RAW_FILE_NAME(Raw file name)=426_2.mzXML
SUBJECT_SAMPLE_FACTORS           	-	426_3	Genotype:WT | Treatment:Control for Overexpression | Sample source:iPSC	RAW_FILE_NAME(Raw file name)=426_3.mzXML
SUBJECT_SAMPLE_FACTORS           	-	426_4	Genotype:WT | Treatment:Control for Overexpression | Sample source:iPSC	RAW_FILE_NAME(Raw file name)=426_4.mzXML
SUBJECT_SAMPLE_FACTORS           	-	426_5	Genotype:WT | Treatment:Control for Overexpression | Sample source:iPSC	RAW_FILE_NAME(Raw file name)=426_5.mzXML
SUBJECT_SAMPLE_FACTORS           	-	LPL_1	Genotype:WT | Treatment:LPL Overexpress | Sample source:iPSC	RAW_FILE_NAME(Raw file name)=LPL_1.mzXML
SUBJECT_SAMPLE_FACTORS           	-	LPL_2	Genotype:WT | Treatment:LPL Overexpress | Sample source:iPSC	RAW_FILE_NAME(Raw file name)=LPL_2.mzXML
SUBJECT_SAMPLE_FACTORS           	-	LPL_3	Genotype:WT | Treatment:LPL Overexpress | Sample source:iPSC	RAW_FILE_NAME(Raw file name)=LPL_3.mzXML
SUBJECT_SAMPLE_FACTORS           	-	LPL_4	Genotype:WT | Treatment:LPL Overexpress | Sample source:iPSC	RAW_FILE_NAME(Raw file name)=LPL_4.mzXML
SUBJECT_SAMPLE_FACTORS           	-	LPL_5	Genotype:WT | Treatment:LPL Overexpress | Sample source:iPSC	RAW_FILE_NAME(Raw file name)=LPL_5.mzXML
SUBJECT_SAMPLE_FACTORS           	-	TSC_1	Genotype:TSC mutation | Treatment:Control for Knockdown | Sample source:iPSC	RAW_FILE_NAME(Raw file name)=TSC_1.mzXML
SUBJECT_SAMPLE_FACTORS           	-	TSC_2	Genotype:TSC mutation | Treatment:Control for Knockdown | Sample source:iPSC	RAW_FILE_NAME(Raw file name)=TSC_1.mzXML
SUBJECT_SAMPLE_FACTORS           	-	TSC_3	Genotype:TSC mutation | Treatment:Control for Knockdown | Sample source:iPSC	RAW_FILE_NAME(Raw file name)=TSC_1.mzXML
SUBJECT_SAMPLE_FACTORS           	-	TSC_4	Genotype:TSC mutation | Treatment:Control for Knockdown | Sample source:iPSC	RAW_FILE_NAME(Raw file name)=TSC_1.mzXML
SUBJECT_SAMPLE_FACTORS           	-	TSC_5	Genotype:TSC mutation | Treatment:Control for Knockdown | Sample source:iPSC	RAW_FILE_NAME(Raw file name)=TSC_1.mzXML
SUBJECT_SAMPLE_FACTORS           	-	KD_1	Genotype:TSC mutation | Treatment:LPL knockdown | Sample source:iPSC	RAW_FILE_NAME(Raw file name)=KD_1.mzXML
SUBJECT_SAMPLE_FACTORS           	-	KD_2	Genotype:TSC mutation | Treatment:LPL knockdown | Sample source:iPSC	RAW_FILE_NAME(Raw file name)=KD_2.mzXML
SUBJECT_SAMPLE_FACTORS           	-	KD_3	Genotype:TSC mutation | Treatment:LPL knockdown | Sample source:iPSC	RAW_FILE_NAME(Raw file name)=KD_3.mzXML
SUBJECT_SAMPLE_FACTORS           	-	KD_4	Genotype:TSC mutation | Treatment:LPL knockdown | Sample source:iPSC	RAW_FILE_NAME(Raw file name)=KD_4.mzXML
SUBJECT_SAMPLE_FACTORS           	-	KD_5	Genotype:TSC mutation | Treatment:LPL knockdown | Sample source:iPSC	RAW_FILE_NAME(Raw file name)=KD_5.mzXML
#COLLECTION
CO:COLLECTION_SUMMARY            	Cell line and sample collection were done at Emory University All iPSC lines
CO:COLLECTION_SUMMARY            	have been fully characterized and cultured on Corning matrigel matrix (Corning,
CO:COLLECTION_SUMMARY            	354234) coated plates in human iPSC mTeSR™1 media (Stemcell, 85850).
CO:COLLECTION_SUMMARY            	hiPSC-microglia were generated using microglia differentiation media and
CO:COLLECTION_SUMMARY            	microglia mature media. 2 million microglia cells were collected for each sample
CO:SAMPLE_TYPE                   	Microglia
#TREATMENT
TR:TREATMENT_SUMMARY             	LPL overexpression and knockdown were achieved through lentivirus infection. LPL
TR:TREATMENT_SUMMARY             	overexpression in a control cell line and knockdown in a TSC cell line were
TR:TREATMENT_SUMMARY             	validated by qPCR and bulk RNA-RNAseq.
#SAMPLEPREP
SP:SAMPLEPREP_SUMMARY            	Lipids were extracted from cell by cold isopropanol (10:1 v/v, solvent to
SP:SAMPLEPREP_SUMMARY            	sample). Extracted lipids were dried under nitrogen gas, resuspended in 65%
SP:SAMPLEPREP_SUMMARY            	acetonitrile, 30% isopropanol and 5% water.
#CHROMATOGRAPHY
CH:CHROMATOGRAPHY_TYPE           	Reversed phase
CH:INSTRUMENT_NAME               	Waters NanoAcquity
CH:COLUMN_NAME                   	Ascentis Express C18 column, 2.7um, 90A, 15cm × 300µm
CH:SOLVENT_A                     	60% water/40% acetonitrile; 10 mM ammonium formate; 0.1% formic acid
CH:SOLVENT_B                     	90% isopropanol/10% acetonitrile; 10 mM ammonium formate; 0.1% formic acid
CH:FLOW_GRADIENT                 	10-75%B in 34min
CH:FLOW_RATE                     	-
CH:COLUMN_TEMPERATURE            	RT
#ANALYSIS
AN:ANALYSIS_TYPE                 	MS
#MS
MS:INSTRUMENT_NAME               	Thermo Q Exactive HF hybrid Orbitrap
MS:INSTRUMENT_TYPE               	Orbitrap
MS:MS_TYPE                       	ESI
MS:ION_MODE                      	POSITIVE
MS:MS_COMMENTS                   	MS1:120k resolution, 100-1200 m/z, 3e6 AGC, 50 ms maximal ion time MS2:top 20,
MS:MS_COMMENTS                   	30k resolution, 2e5 AGC, 45 ms maximal ion time, stepped HCD NCE at 30, 75, 150
MS:MS_COMMENTS                   	In-house JUMPm software and Shiny were used for data processing, feature
MS:MS_COMMENTS                   	assignment and statistic analysis
MS:MS_RESULTS_FILE               	ST003352_AN005493_Results.txt	UNITS:Intensity	Has m/z:Yes	Has RT:Yes	RT units:Minutes
#END