Summary of Study ST001810

This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench, https://www.metabolomicsworkbench.org, where it has been assigned Project ID PR001144. The data can be accessed directly via it's Project DOI: 10.21228/M8TQ3Q This work is supported by NIH grant, U2C- DK119886.

See: https://www.metabolomicsworkbench.org/about/howtocite.php

This study contains a large results data set and is not available in the mwTab file. It is only available for download via FTP as data file(s) here.

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Study IDST001810
Study TitleMetabolomics-driven identification of biochemical mechanisms underlying the neuroprotective effects of pleiotrophin in a mouse model of Parkinson’s disease
Study SummaryPleiotrophin (PTN) is a cytokine involved in nerve tissue repair processes, neuroinflammation and neuronal survival. PTN expression levels are upregulated in the nigrostriatal pathway of Parkinson’s Disease (PD) patients. We aimed to characterize the dopaminergic injury and glial activation in the nigrostriatal pathway of mice with transgenic Ptn overexpression in the brain (Ptn-Tg) after intrastriatal injection of the Parkinsonian toxin 6-hydroxydopamine (6-OHDA). The injection of 6-OHDA induced a significant decrease of the number of tyrosine hydroxylase (TH)-positive neurons in the substantia nigra and of the striatal TH contents in Wild type (Wt) mice. In contrast, these effects of 6-OHDA were blocked in Ptn-Tg mice. 6-OHDA injection did not cause robust changes in microglia but induced an exacerbated astrocytic response in Wt mice compared with Ptn-Tg mice. In metabolomics studies, we detected interesting metabolites that significantly discriminate the more injured 6-OHDA-injected Wt striatum and the more protected 6-OHDA-injected Ptn-Tg striatum. Particularly, we detected groups of metabolites, mostly corresponding to phospholipids, whose trends were opposite in both groups. In summary, the data confirm the neuroprotective effect of brain PTN overexpression in this mouse model of PD. New lipid-related PD drug candidates emerge from this study and the data presented here support the increasingly recognized “lipid cascade” in PD.
Institute
CEMBIO
Last NameSáiz
First NameJorge
AddressJULIÁN ROMEA 23, Madrid, Madrid, 28003, Spain
Emailjorge.saizgalindo@ceu.es
Phonenone
Submit Date2021-06-01
Raw Data AvailableYes
Raw Data File Type(s)d
Analysis Type DetailLC-MS
Release Date2021-06-16
Release Version1
Jorge Sáiz Jorge Sáiz
https://dx.doi.org/10.21228/M8TQ3Q
ftp://www.metabolomicsworkbench.org/Studies/ application/zip

Select appropriate tab below to view additional metadata details:

Project:

Project ID:PR001144
Project DOI:doi: 10.21228/M8TQ3Q
Project Title:Metabolomics-driven identification of biochemical mechanisms underlying the neuroprotective effects of pleiotrophin in a mouse model of Parkinson’s disease
Project Summary:Pleiotrophin (PTN) is a cytokine involved in nerve tissue repair processes, neuroinflammation and neuronal survival. PTN expression levels are upregulated in the nigrostriatal pathway of Parkinson’s Disease (PD) patients. We aimed to characterize the dopaminergic injury and glial activation in the nigrostriatal pathway of mice with transgenic Ptn overexpression in the brain (Ptn-Tg) after intrastriatal injection of the Parkinsonian toxin 6-hydroxydopamine (6-OHDA). The injection of 6-OHDA induced a significant decrease of the number of tyrosine hydroxylase (TH)-positive neurons in the substantia nigra and of the striatal TH contents in Wild type (Wt) mice. In contrast, these effects of 6-OHDA were blocked in Ptn-Tg mice. 6-OHDA injection did not cause robust changes in microglia but induced an exacerbated astrocytic response in Wt mice compared with Ptn-Tg mice. In metabolomics studies, we detected interesting metabolites that significantly discriminate the more injured 6-OHDA-injected Wt striatum and the more protected 6-OHDA-injected Ptn-Tg striatum. Particularly, we detected groups of metabolites, mostly corresponding to phospholipids, whose trends were opposite in both groups. In summary, the data confirm the neuroprotective effect of brain PTN overexpression in this mouse model of PD. New lipid-related PD drug candidates emerge from this study and the data presented here support the increasingly recognized “lipid cascade” in PD.
Institute:Universidad CEU San Pablo
Last Name:Sáiz
First Name:Jorge
Address:JULIÁN ROMEA 23, Madrid, Madrid, 28003, Spain
Email:jorge.saizgalindo@ceu.es
Phone:913 72 47 11

Subject:

Subject ID:SU001887
Subject Type:Mammal
Subject Species:Mus musculus
Taxonomy ID:10090

Factors:

Subject type: Mammal; Subject species: Mus musculus (Factor headings shown in green)

mb_sample_id local_sample_id Subject type Treatment
SA168132QC5-POSQC QC
SA168133QC6-POSQC QC
SA168134QC4-POSQC QC
SA168135QC2-POSQC QC
SA168136QC1-POSQC QC
SA168137QC1-NEGQC QC
SA168138QC3-POSQC QC
SA168139QC7-POSQC QC
SA168140QC6-NEGQC QC
SA168141QC7-NEGQC QC
SA168142QC4-NEGQC QC
SA168143QC5-NEGQC QC
SA168144QC3-NEGQC QC
SA168145QC2-NEGQC QC
SA168146T3-HD-NEG.dTransg OH-Dopamine
SA168147T2-HD-NEG.dTransg OH-Dopamine
SA168148T1-HD-NEG.dTransg OH-Dopamine
SA168149T5-HD-NEG.dTransg OH-Dopamine
SA168150T4-HD-NEG.dTransg OH-Dopamine
SA168151T2-HD-POS.dTransg OH-Dopamine
SA168152T3-HD-POS.dTransg OH-Dopamine
SA168153T4-HD-POS.dTransg OH-Dopamine
SA168154T1-HD-POS.dTransg OH-Dopamine
SA168155T5-HD-POS.dTransg OH-Dopamine
SA168156T1-VEH-NEG.dTransg Vehicle
SA168157T7-VEH-NEG.dTransg Vehicle
SA168158T6-VEH-NEG.dTransg Vehicle
SA168159T5-VEH-NEG.dTransg Vehicle
SA168160T6-VEH-POS.dTransg Vehicle
SA168161T7-VEH-POS.dTransg Vehicle
SA168162T4-VEH-NEG.dTransg Vehicle
SA168163T5-VEH-POS.dTransg Vehicle
SA168164T1-VEH-POS.dTransg Vehicle
SA168165T2-VEH-NEG.dTransg Vehicle
SA168166T2-VEH-POS.dTransg Vehicle
SA168167T4-VEH-POS.dTransg Vehicle
SA168168WT8-HD-NEG.dWT OH-Dopamine
SA168169WT7-HD-NEG.dWT OH-Dopamine
SA168170WT9-HD-NEG.dWT OH-Dopamine
SA168171WT11-HD-NEG.dWT OH-Dopamine
SA168172WT6-HD-NEG.dWT OH-Dopamine
SA168173WT12-HD-NEG.dWT OH-Dopamine
SA168174WT10-HD-NEG.dWT OH-Dopamine
SA168175WT1-HD-NEG.dWT OH-Dopamine
SA168176WT9-HD-POS.dWT OH-Dopamine
SA168177WT8-HD-POS.dWT OH-Dopamine
SA168178WT7-HD-POS.dWT OH-Dopamine
SA168179WT10-HD-POS.dWT OH-Dopamine
SA168180WT11-HD-POS.dWT OH-Dopamine
SA168181WT5-HD-NEG.dWT OH-Dopamine
SA168182WT12-HD-POS.dWT OH-Dopamine
SA168183WT5-HD-POS.dWT OH-Dopamine
SA168184WT6-HD-POS.dWT OH-Dopamine
SA168185WT3-HD-NEG.dWT OH-Dopamine
SA168186WT4-HD-NEG.dWT OH-Dopamine
SA168187WT2-HD-NEG.dWT OH-Dopamine
SA168188WT1-HD-POS.dWT OH-Dopamine
SA168189WT4-HD-POS.dWT OH-Dopamine
SA168190WT3-HD-POS.dWT OH-Dopamine
SA168191WT2-HD-POS.dWT OH-Dopamine
SA168192WT2-VEH-POS.dWT Vehicle
SA168193WT1-VEH-POS.dWT Vehicle
SA168194WT3-VEH-POS.dWT Vehicle
SA168195WT7-VEH-NEG.dWT Vehicle
SA168196WT6-VEH-POS.dWT Vehicle
SA168197WT4-VEH-POS.dWT Vehicle
SA168198WT7-VEH-POS.dWT Vehicle
SA168199WT8-VEH-POS.dWT Vehicle
SA168200WT10-VEH-POS.dWT Vehicle
SA168201WT9-VEH-POS.dWT Vehicle
SA168202WT1-VEH-NEG.dWT Vehicle
SA168203WT2-VEH-NEG.dWT Vehicle
SA168204WT8-VEH-NEG.dWT Vehicle
SA168205WT9-VEH-NEG.dWT Vehicle
SA168206WT6-VEH-NEG.dWT Vehicle
SA168207WT4-VEH-NEG.dWT Vehicle
SA168208WT3-VEH-NEG.dWT Vehicle
SA168209WT10-VEH-NEG.dWT Vehicle
Showing results 1 to 78 of 78

Collection:

Collection ID:CO001880
Collection Summary:Samples were collected and frozen at -80ºC
Sample Type:Brain

Treatment:

Treatment ID:TR001900
Treatment Summary:Striatum resections were added to 300 µL MeOH:water (50:50) in 2 mL Eppendorf tubes and were first homogenized with glass beads in a TissueLyser LT (QIAGEN) for 2 min. The tubes were immersed in liquid N2 and homogenized again in the TissueLyser LT for another 2 min. A volume 100 µL of the homogenate was transferred into Eppendorf tubes of 1.5 mL and added with 320 µL of methanol and 80 µL of MTBE and the mixture was vortexed for 1 h. Afterwards, the vials were centrifuged at 4000 g for 20 min at 20 ºC and 300 µL of the supernatants were transferred into new tubes, which were evaporated to dryness in a vacuum concentrator. Finally, the residues were reconstituted in 50 µL of MeOH:water:MTBE (37:5:4), being the samples ready for their analysis. Blank samples were prepared following the sample procedure without the addition of any biological tissue.

Sample Preparation:

Sampleprep ID:SP001893
Sampleprep Summary:Striatum resections were added to 300 µL MeOH:water (50:50) in 2 mL Eppendorf tubes and were first homogenized with glass beads in a TissueLyser LT (QIAGEN) for 2 min. The tubes were immersed in liquid N2 and homogenized again in the TissueLyser LT for another 2 min. A volume 100 µL of the homogenate was transferred into Eppendorf tubes of 1.5 mL and added with 320 µL of methanol and 80 µL of MTBE and the mixture was vortexed for 1 h. Afterwards, the vials were centrifuged at 4000 g for 20 min at 20 ºC and 300 µL of the supernatants were transferred into new tubes, which were evaporated to dryness in a vacuum concentrator. Finally, the residues were reconstituted in 50 µL of MeOH:water:MTBE (37:5:4), being the samples ready for their analysis. Blank samples were prepared following the sample procedure without the addition of any biological tissue.

Combined analysis:

Analysis ID AN002933 AN002934
Analysis type MS MS
Chromatography type Reversed phase Reversed phase
Chromatography system Agilent 1200 Agilent 1200
Column RP C8 Agilent Poroshell (150 x 2.1mm,2.7um) RP C8 Agilent Poroshell (150 x 2.1mm,2.7um)
MS Type ESI ESI
MS instrument type QTOF QTOF
MS instrument name Agilent 6520 QTOF Agilent 6520 QTOF
Ion Mode POSITIVE NEGATIVE
Units aera area

Chromatography:

Chromatography ID:CH002174
Instrument Name:Agilent 1200
Column Name:RP C8 Agilent Poroshell (150 x 2.1mm,2.7um)
Chromatography Type:Reversed phase

MS:

MS ID:MS002724
Analysis ID:AN002933
Instrument Name:Agilent 6520 QTOF
Instrument Type:QTOF
MS Type:ESI
MS Comments:All data were controlled and acquired using Mass Hunter Qualitative Analysis B.07.00 (Agilent Technologies). Data obtained from LC-MS were cleaned of background noise and unrelated ions. Peak detection, deconvolution and alignment were performed by the recursive feature extraction (RFE) using Profinder Software B.08.00 (Agilent Technologies). Blank subtraction and filtering by frequency of at least 50% of the QC and 60% of each group and relative standard deviation (RSD) less than 30% in QC were performed, to keep only the relevant features. Missing values were substituted by KNN algorithm.
Ion Mode:POSITIVE
  
MS ID:MS002725
Analysis ID:AN002934
Instrument Name:Agilent 6520 QTOF
Instrument Type:QTOF
MS Type:ESI
MS Comments:All data were controlled and acquired using Mass Hunter Qualitative Analysis B.07.00 (Agilent Technologies). Data obtained from LC-MS were cleaned of background noise and unrelated ions. Peak detection, deconvolution and alignment were performed by the recursive feature extraction (RFE) using Profinder Software B.08.00 (Agilent Technologies). Blank subtraction and filtering by frequency of at least 50% of the QC and 60% of each group and relative standard deviation (RSD) less than 30% in QC were performed, to keep only the relevant features. Missing values were substituted by KNN algorithm.
Ion Mode:NEGATIVE
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