#METABOLOMICS WORKBENCH silviaradenkovic_20230418_110829 DATATRACK_ID:3868 STUDY_ID:ST002564 ANALYSIS_ID:AN004225 PROJECT_ID:PR001653
VERSION             	1
CREATED_ON             	April 18, 2023, 4:51 pm
#PROJECT
PR:PROJECT_TITLE                 	Metabolomic profiling of PMM2-CDG after siRNA mediated KD of AKR1b1 and
PR:PROJECT_TITLE                 	neuraminidase treatment
PR:PROJECT_SUMMARY               	Abnormal polyol metabolism has been predominantly associated with diabetes,
PR:PROJECT_SUMMARY               	where excess glucose is converted to sorbitol by aldose reductase (AR).
PR:PROJECT_SUMMARY               	Recently, abnormal polyol metabolism has also been implicated in
PR:PROJECT_SUMMARY               	phosphomannomutase 2-congenital disorder of glycosylation (PMM2-CDG), and
PR:PROJECT_SUMMARY               	epalrestat, an AR inhibitor, proposed as a potential therapy for this disorder.
PR:PROJECT_SUMMARY               	Given that the PMM enzyme is not closely connected to polyol metabolism, and,
PR:PROJECT_SUMMARY               	unlike in diabetes, PMM2-CDG does not present with hyperglycemia in blood, the
PR:PROJECT_SUMMARY               	increased polyol production, and the therapeutic mechanism of epalrestat in
PR:PROJECT_SUMMARY               	PMM2-CDG remained largely elusive. PMM2-CDG is caused by deficiency of the PMM
PR:PROJECT_SUMMARY               	enzyme and results in a depletion of mannose-1-P and guanosine diphosphate
PR:PROJECT_SUMMARY               	mannose (GDP-mannose), which is essential for glycosylation. Here, we show that
PR:PROJECT_SUMMARY               	apart from glycosylation abnormalities, PMM2 deficiency also leads to changes in
PR:PROJECT_SUMMARY               	intracellular glucose flux, which results in an increase in intracellular
PR:PROJECT_SUMMARY               	polyols. Ssing tracer glucose studies, we demonstrate that AR inhibition diverts
PR:PROJECT_SUMMARY               	glucose flux away from polyol production towards the synthesis of sugar
PR:PROJECT_SUMMARY               	nucleotides, which results in increase in glucose flux towards glycans.
PR:INSTITUTE                     	Mayo Clinic
PR:LAST_NAME                     	Radenkovic
PR:FIRST_NAME                    	Silvia
PR:ADDRESS                       	200 2nd Ave SW Rochester MN
PR:EMAIL                         	radenkovic.silvia@mayo.edu
PR:PHONE                         	507(77) 6-6107
PR:FUNDING_SOURCE                	NIH, KU Leuven
#STUDY
ST:STUDY_TITLE                   	Metabolomic profiling of PMM2-CDG after siRNA mediated KD of AKR1b1 and
ST:STUDY_TITLE                   	neuraminidase treatment
ST:STUDY_SUMMARY                 	Abnormal polyol metabolism has been predominantly associated with diabetes,
ST:STUDY_SUMMARY                 	where excess glucose is converted to sorbitol by aldose reductase (AR).
ST:STUDY_SUMMARY                 	Recently, abnormal polyol metabolism has also been implicated in
ST:STUDY_SUMMARY                 	phosphomannomutase 2-congenital disorder of glycosylation (PMM2-CDG), and
ST:STUDY_SUMMARY                 	epalrestat, an AR inhibitor, proposed as a potential therapy for this disorder.
ST:STUDY_SUMMARY                 	Given that the PMM enzyme is not closely connected to polyol metabolism, and,
ST:STUDY_SUMMARY                 	unlike in diabetes, PMM2-CDG does not present with hyperglycemia in blood, the
ST:STUDY_SUMMARY                 	increased polyol production, and the therapeutic mechanism of epalrestat in
ST:STUDY_SUMMARY                 	PMM2-CDG remained largely elusive. PMM2-CDG is caused by deficiency of the PMM
ST:STUDY_SUMMARY                 	enzyme and results in a depletion of mannose-1-P and guanosine diphosphate
ST:STUDY_SUMMARY                 	mannose (GDP-mannose), which is essential for glycosylation. Here, we show that
ST:STUDY_SUMMARY                 	apart from glycosylation abnormalities, PMM2 deficiency also leads to changes in
ST:STUDY_SUMMARY                 	intracellular glucose flux, which results in an increase in intracellular
ST:STUDY_SUMMARY                 	polyols. Ssing tracer glucose studies, we demonstrate that AR inhibition diverts
ST:STUDY_SUMMARY                 	glucose flux away from polyol production towards the synthesis of sugar
ST:STUDY_SUMMARY                 	nucleotides, which results in increase in glucose flux towards glycans.
ST:INSTITUTE                     	Mayo Clinic
ST:LAST_NAME                     	Radenkovic
ST:FIRST_NAME                    	Silvia
ST:ADDRESS                       	200 2nd Ave SW Rochester MN, USA
ST:EMAIL                         	radenkovic.silvia@mayo.edu
ST:PHONE                         	507(77) 6-6107
#SUBJECT
SU:SUBJECT_TYPE                  	Cultured cells
SU:SUBJECT_SPECIES               	Homo sapiens
SU:TAXONOMY_ID                   	9606
SU:GENOTYPE_STRAIN               	WT/PMM2-CDG
SU:AGE_OR_AGE_RANGE              	5-45
SU:GENDER                        	Male and female
#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           	P2	SR01	Genotype:PMM2-CDG | Treatment:5.5mM 13C GLU  negative siRNA	Organism=Homo sapiens; Tissue type=Fibroblasts; RAW_FILE_NAME=SR01
SUBJECT_SAMPLE_FACTORS           	P2	SR02	Genotype:PMM2-CDG | Treatment:5.5mM 12C GLU  negative siRNA	Organism=Homo sapiens; Tissue type=Fibroblasts; RAW_FILE_NAME=SR02
SUBJECT_SAMPLE_FACTORS           	P2	SR03	Genotype:PMM2-CDG | Treatment:5.5mM 13C GLU  siRNA	Organism=Homo sapiens; Tissue type=Fibroblasts; RAW_FILE_NAME=SR03
SUBJECT_SAMPLE_FACTORS           	P2	SR04	Genotype:PMM2-CDG | Treatment:5.5mM 12C GLU  siRNA	Organism=Homo sapiens; Tissue type=Fibroblasts; RAW_FILE_NAME=SR04
SUBJECT_SAMPLE_FACTORS           	P5	SR05	Genotype:PMM2-CDG | Treatment:5.5mM 13C GLU  negative siRNA	Organism=Homo sapiens; Tissue type=Fibroblasts; RAW_FILE_NAME=SR05
SUBJECT_SAMPLE_FACTORS           	P5	SR06	Genotype:PMM2-CDG | Treatment:5.5mM 12C GLU  negative siRNA	Organism=Homo sapiens; Tissue type=Fibroblasts; RAW_FILE_NAME=SR06
SUBJECT_SAMPLE_FACTORS           	P5	SR07	Genotype:PMM2-CDG | Treatment:5.5mM 13C GLU  siRNA	Organism=Homo sapiens; Tissue type=Fibroblasts; RAW_FILE_NAME=SR07
SUBJECT_SAMPLE_FACTORS           	P5	SR08	Genotype:PMM2-CDG | Treatment:5.5mM 12C GLU  siRNA	Organism=Homo sapiens; Tissue type=Fibroblasts; RAW_FILE_NAME=SR08
SUBJECT_SAMPLE_FACTORS           	C3	SR09	Genotype:WT | Treatment:5.5mM 13C GLU  negative siRNA	Organism=Homo sapiens; Tissue type=Fibroblasts; RAW_FILE_NAME=SR09
SUBJECT_SAMPLE_FACTORS           	C3	SR10	Genotype:WT | Treatment:5.5mM 12C GLU  negative siRNA	Organism=Homo sapiens; Tissue type=Fibroblasts; RAW_FILE_NAME=SR10
SUBJECT_SAMPLE_FACTORS           	C3	SR11	Genotype:WT | Treatment:5.5mM 13C GLU  siRNA	Organism=Homo sapiens; Tissue type=Fibroblasts; RAW_FILE_NAME=SR11
SUBJECT_SAMPLE_FACTORS           	C3	SR12	Genotype:WT | Treatment:5.5mM 12C GLU  siRNA	Organism=Homo sapiens; Tissue type=Fibroblasts; RAW_FILE_NAME=SR12
SUBJECT_SAMPLE_FACTORS           	C2	SR13	Genotype:WT | Treatment:5.5mM 13C GLU  negative siRNA	Organism=Homo sapiens; Tissue type=Fibroblasts; RAW_FILE_NAME=SR13
SUBJECT_SAMPLE_FACTORS           	C2	SR14	Genotype:WT | Treatment:5.5mM 12C GLU  negative siRNA	Organism=Homo sapiens; Tissue type=Fibroblasts; RAW_FILE_NAME=SR14
SUBJECT_SAMPLE_FACTORS           	C2	SR15	Genotype:WT | Treatment:5.5mM 13C GLU  siRNA	Organism=Homo sapiens; Tissue type=Fibroblasts; RAW_FILE_NAME=SR15
SUBJECT_SAMPLE_FACTORS           	C2	SR16	Genotype:WT | Treatment:5.5mM 12C GLU  siRNA	Organism=Homo sapiens; Tissue type=Fibroblasts; RAW_FILE_NAME=SR16
#COLLECTION
CO:COLLECTION_SUMMARY            	Briefly, medium was removed from the cells and the cells were washed 3 times
CO:COLLECTION_SUMMARY            	with 1 mL Dulbecco PBS containing 0.901 mM CaCl2 (Merck) and 0.492 mM MgCl2
CO:COLLECTION_SUMMARY            	(Merck). Next, cells were incubated with 1 mg/100 mL EZ-Link-Sulfo-NHS-LC-Biotin
CO:COLLECTION_SUMMARY            	(Thermo) in Dulbecco for 30 min, RT, shaking. Cells were then washed twice with
CO:COLLECTION_SUMMARY            	1 mL Dulbecco, non-reacted biotin was blocked with 1 mL 20 mM glycine in
CO:COLLECTION_SUMMARY            	Dulbecco for 15 min, and cells washed again with 1 mL Dulbecco. Dulbecco was
CO:COLLECTION_SUMMARY            	then removed, cells scraped in 200 µL RIPA buffer (with protease inhibitors)
CO:COLLECTION_SUMMARY            	and transferred to a fresh Eppendorf tube. Samples were lysed on ice with 3
CO:COLLECTION_SUMMARY            	consecutive freeze-thaw cycles. Further, 30 µL dynabeads streptavidin T1
CO:COLLECTION_SUMMARY            	(Invitrogen) was added to each sample and the samples were washed twice with 500
CO:COLLECTION_SUMMARY            	µL 10 mM ammonium bicarbonate and neuraminidase buffer (100 mM Sodium Acetate
CO:COLLECTION_SUMMARY            	Buffer with 2 mM CaCl2 (Merck), pH 5.0). Neuraminidase buffer was removed and
CO:COLLECTION_SUMMARY            	500 µL PBS was added to the beads. 30 µL of prepared mix was added to each
CO:COLLECTION_SUMMARY            	sample, and samples were incubated, shaking overnight at 4 °C. Samples were put
CO:COLLECTION_SUMMARY            	on a dynabead rack (Invitrogen) and the supernatant was transferred to a new
CO:COLLECTION_SUMMARY            	Eppendorf tube and used for protein concentration assay. Beads containing
CO:COLLECTION_SUMMARY            	membrane fractions were washed 2 times with 500 µL lysis buffer (2 % IGEPAL
CO:COLLECTION_SUMMARY            	(Sigma), 1% Triton X-100 (Sigma), and 10 % glycerol inPBS) and then washed with
CO:COLLECTION_SUMMARY            	1 mL PBS. Samples are centrifuged at 500 rcf, 5 min, 4 °C and PBS was removed.
CO:COLLECTION_SUMMARY            	100 µL neuraminidase buffer containing 0.05 U neuraminidase was added to each
CO:COLLECTION_SUMMARY            	sample and samples were incubated overnight at 37 °C, shaking. Next,
CO:COLLECTION_SUMMARY            	supernatant was transferred to a new Eppendorf tube and lyophilized at 4 °C.
CO:COLLECTION_SUMMARY            	Finally, pellets were resuspended in 100 µL of extraction buffer (80 % MeOH,
CO:COLLECTION_SUMMARY            	IS). Sialic acid was measured by LC/MS as described below. El Maven Polly
CO:COLLECTION_SUMMARY            	software was used to annotate sialic acid based on m/z ratio and elution time,
CO:COLLECTION_SUMMARY            	and determine fractional contribution of glucose in sialic acid.
CO:SAMPLE_TYPE                   	Fibroblasts
CO:STORAGE_CONDITIONS            	-80℃
#TREATMENT
TR:TREATMENT_SUMMARY             	Cells were treated with vehicle or 5nM siRNA targeting AKR1B1, Before
TR:TREATMENT_SUMMARY             	collection, medium was removed from the cells and the cells were washed 3 times
TR:TREATMENT_SUMMARY             	with 1 mL Dulbecco PBS containing 0.901 mM CaCl2 (Merck) and 0.492 mM MgCl2
TR:TREATMENT_SUMMARY             	(Merck). Next, cells were incubated with 1 mg/100 mL EZ-Link-Sulfo-NHS-LC-Biotin
TR:TREATMENT_SUMMARY             	(Thermo) in Dulbecco for 30 min, RT, shaking. Cells were then washed twice with
TR:TREATMENT_SUMMARY             	1 mL Dulbecco, non-reacted biotin was blocked with 1 mL 20 mM glycine in
TR:TREATMENT_SUMMARY             	Dulbecco for 15 min, and cells washed again with 1 mL Dulbecco. Dulbecco was
TR:TREATMENT_SUMMARY             	then removed, cells scraped in 200 µL RIPA buffer (with protease inhibitors)
TR:TREATMENT_SUMMARY             	and transferred to a fresh Eppendorf tube. Samples were lysed on ice with 3
TR:TREATMENT_SUMMARY             	consecutive freeze-thaw cycles. Further, 30 µL dynabeads streptavidin T1
TR:TREATMENT_SUMMARY             	(Invitrogen) was added to each sample and the samples were washed twice with 500
TR:TREATMENT_SUMMARY             	µL 10 mM ammonium bicarbonate and neuraminidase buffer (100 mM Sodium Acetate
TR:TREATMENT_SUMMARY             	Buffer with 2 mM CaCl2 (Merck), pH 5.0). Neuraminidase buffer was removed and
TR:TREATMENT_SUMMARY             	500 µL PBS was added to the beads. 30 µL of prepared mix was added to each
TR:TREATMENT_SUMMARY             	sample, and samples were incubated, shaking overnight at 4 °C. Samples were put
TR:TREATMENT_SUMMARY             	on a dynabead rack (Invitrogen) and the supernatant was transferred to a new
TR:TREATMENT_SUMMARY             	Eppendorf tube and used for protein concentration assay. Beads containing
TR:TREATMENT_SUMMARY             	membrane fractions were washed 2 times with 500 µL lysis buffer (2 % IGEPAL
TR:TREATMENT_SUMMARY             	(Sigma), 1% Triton X-100 (Sigma), and 10 % glycerol inPBS) and then washed with
TR:TREATMENT_SUMMARY             	1 mL PBS. Samples are centrifuged at 500 rcf, 5 min, 4 °C and PBS was removed.
TR:TREATMENT_SUMMARY             	100 µL neuraminidase buffer containing 0.05 U neuraminidase was added to each
TR:TREATMENT_SUMMARY             	sample and samples were incubated overnight at 37 °C, shaking. Next,
TR:TREATMENT_SUMMARY             	supernatant was transferred to a new Eppendorf tube and lyophilized at 4 °C.
TR:TREATMENT_SUMMARY             	Finally, pellets were resuspended in 100 µL of extraction buffer (80 % MeOH,
TR:TREATMENT_SUMMARY             	IS). Sialic acid was measured by LC/MS as described below. El Maven Polly
TR:TREATMENT_SUMMARY             	software was used to annotate sialic acid based on m/z ratio and elution time,
TR:TREATMENT_SUMMARY             	and determine fractional contribution of glucose in sialic acid.
#SAMPLEPREP
SP:SAMPLEPREP_SUMMARY            	After treatment with neuraminidase, supernatant was transferred to a new
SP:SAMPLEPREP_SUMMARY            	Eppendorf tube and lyophilized at 4 °C. Finally, lyophilized pellets were
SP:SAMPLEPREP_SUMMARY            	resuspended in 100 µL of extraction buffer (80 % MeOH, IS).
SP:PROCESSING_STORAGE_CONDITIONS 	-80℃
SP:EXTRACT_STORAGE               	-80℃
#CHROMATOGRAPHY
CH:CHROMATOGRAPHY_SUMMARY        	C18 iP REVERSE PHASE
CH:CHROMATOGRAPHY_TYPE           	Reversed phase
CH:INSTRUMENT_NAME               	Waters Acquity
CH:COLUMN_NAME                   	Waters ACQUITY UPLC HSS T3 (150 x 2.1mm,1.8um)
CH:SOLVENT_A                     	100% water; 10mM tributylamine; 15mM acetic acid
CH:SOLVENT_B                     	100% methanol
CH:FLOW_GRADIENT                 	The gradient started with 5% of solvent B and 95% solvent A and remained at 5% B
CH:FLOW_GRADIENT                 	until 2 min post injection. A linear gradient to 37% B was carried out until 7
CH:FLOW_GRADIENT                 	min and increased to 41% until 14 min. Between 14 and 26 minutes the gradient
CH:FLOW_GRADIENT                 	increased to 95% of B and remained at 95% B for 4 minutes. At 30 min the
CH:FLOW_GRADIENT                 	gradient returned to 5% B. The chromatography was stopped at 40 min.
CH:FLOW_RATE                     	0.25 mL/min
CH:COLUMN_TEMPERATURE            	40
#ANALYSIS
AN:ANALYSIS_TYPE                 	MS
#MS
MS:INSTRUMENT_NAME               	Thermo Q Exactive Orbitrap
MS:INSTRUMENT_TYPE               	Orbitrap
MS:MS_TYPE                       	ESI
MS:ION_MODE                      	NEGATIVE
MS:MS_COMMENTS                   	El-Maven polly, ThermoFisher Xcalibur; Sialic acid was annotated using the
MS:MS_COMMENTS                   	inhouse standard metabolite library- elution time and m/z values.
#MS_METABOLITE_DATA
MS_METABOLITE_DATA:UNITS	AUC
MS_METABOLITE_DATA_START
Samples	SR01	SR02	SR03	SR04	SR05	SR06	SR07	SR08	SR09	SR10	SR11	SR12	SR13	SR14	SR15	SR16
Factors	Genotype:PMM2-CDG | Treatment:5.5mM 13C GLU  negative siRNA	Genotype:PMM2-CDG | Treatment:5.5mM 12C GLU  negative siRNA	Genotype:PMM2-CDG | Treatment:5.5mM 13C GLU  siRNA	Genotype:PMM2-CDG | Treatment:5.5mM 12C GLU  siRNA	Genotype:PMM2-CDG | Treatment:5.5mM 13C GLU  negative siRNA	Genotype:PMM2-CDG | Treatment:5.5mM 12C GLU  negative siRNA	Genotype:PMM2-CDG | Treatment:5.5mM 13C GLU  siRNA	Genotype:PMM2-CDG | Treatment:5.5mM 12C GLU  siRNA	Genotype:WT | Treatment:5.5mM 13C GLU  negative siRNA	Genotype:WT | Treatment:5.5mM 12C GLU  negative siRNA	Genotype:WT | Treatment:5.5mM 13C GLU  siRNA	Genotype:WT | Treatment:5.5mM 12C GLU  siRNA	Genotype:WT | Treatment:5.5mM 13C GLU  negative siRNA	Genotype:WT | Treatment:5.5mM 12C GLU  negative siRNA	Genotype:WT | Treatment:5.5mM 13C GLU  siRNA	Genotype:WT | Treatment:5.5mM 12C GLU  siRNA
Sialic acid	1.68E+08	1.57E+08	1.40E+08	1.38E+08	1.65E+08	1.94E+08	2.42E+08	2.88E+08	2.28E+08	1.68E+08	2.65E+08	3.21E+08	1.48E+08	1.73E+08	1.24E+08	1.71E+08
MS_METABOLITE_DATA_END
#METABOLITES
METABOLITES_START
metabolite_name	parent formula	M/Z	HMDB ID	isotopeLabel	isotope count
Sialic acid	C11H19NO9	308.09845	HMDB00230	C12 PARENT	m0-m11
METABOLITES_END
#END