Summary of Study ST003534

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 PR002168. The data can be accessed directly via it's Project DOI: 10.21228/M8CR8X This work is supported by NIH grant, U2C- DK119886.

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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 IDST003534
Study TitleMetabolomic analysis of altered arachidonic acid metabolism in mouse heart tissue after myocardial infarction
Study SummaryWe performed myocardial infarction surgery on wild-type (WT) mice and collected cardiac tissues from the sham group and 1, 7, 14 and 28 days after surgery for LC-MS analysis. The results showed that AA-derived LTB4 was produced in large quantities 2 weeks after myocardial infarction and remained at a high level for a long time.
Institute
Tianjin Medical University
Last NameSong
First NameJiawei
AddressTianjin Medical University, Tianjin, China., Tianjin, Tianjin, 300070, China
Emailsjw808@tmu.edu.cn
Phone15309216256
Submit Date2024-10-22
Raw Data AvailableYes
Raw Data File Type(s)mzML
Analysis Type DetailLC-MS
Release Date2025-11-14
Release Version1
Jiawei Song Jiawei Song
https://dx.doi.org/10.21228/M8CR8X
ftp://www.metabolomicsworkbench.org/Studies/ application/zip

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Project:

Project ID:PR002168
Project DOI:doi: 10.21228/M8CR8X
Project Title:Arachidonic acid fuels inflammation by unlocking 5-LOX in macrophages after myocardial infarction to promote cardiac dysfunction
Project Summary:An overactive inflammatory response and immune cell infiltration in myocardial infarction (MI) impairs tissue repair. Arachidonic acid (AA) metabolites act as important sources of inflammatory mediators in cardiac tissue. We investigated the mechanisms underlying the AA cascade-mediated inflammatory response after MI. Metabolomics analyses revealed that the 5-lipoxygenase (5-LOX)-dependent AA metabolic pathway derivative leukotriene B4 (LTB4) accumulated in large quantities after MI. Elevated levels of AA in vivo after MI facilitated the recruitment of protein phosphatase 5 (PP5) into the nucleus by binding PP5 to its nuclear transporter receptor karyopherin subunit alpha 1. On entering the nucleus, PP5 directly dephosphorylated 5-LOX at Thr218, promoting the production of the proinflammatory mediator LTB4 by macrophages. Transgenic mice were created with a population of cardiac resident macrophages with a mutation at 5-LOX Thr218. Single-cell transcriptomics showed that these cells overexpressed CXC-chemokine ligand 13 and actively recruited B cells to the heart, exacerbating tissue inflammation. In a UK Biobank cohort, the PP5 E76D mutation was found to be associated with complications after acute MI. Overall, our results have elucidated a conserved role for 5-LOX-phosphorylation-regulated LTB4 levels in MI and identified PP5 as a potential therapeutic target for the treatment of MI.
Institute:Tianjin Medical University
Last Name:Song
First Name:Jiawei
Address:Tianjin Medical University, Tianjin, China., Tianjin, Tianjin, 300070, China
Email:sjw808@tmu.edu.cn
Phone:15309216256

Subject:

Subject ID:SU003663
Subject Type:Mammal
Subject Species:Mus musculus
Taxonomy ID:10090
Species Group:Mammals

Factors:

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

mb_sample_id local_sample_id treatment
SA387390MI0d_02post-MI day0
SA387391MI0d_07_arachidonic acidpost-MI day0
SA387392MI0d_06_arachidonic acidpost-MI day0
SA387393MI0d_05_arachidonic acidpost-MI day0
SA387394MI0d_04_arachidonic acidpost-MI day0
SA387395MI0d_03_arachidonic acidpost-MI day0
SA387396MI0d_02_arachidonic acidpost-MI day0
SA387397MI0d_01post-MI day0
SA387398MI0d_01_arachidonic acidpost-MI day0
SA387399MI0d_07post-MI day0
SA387400MI0d_03post-MI day0
SA387401MI0d_05post-MI day0
SA387402MI0d_06post-MI day0
SA387403MI0d_04post-MI day0
SA387418MI1d_04_arachidonic acidpost-MI day1
SA387419MI1d_01_arachidonic acidpost-MI day1
SA387420MI1d_03_arachidonic acidpost-MI day1
SA387421MI1d_03post-MI day1
SA387422MI1d_05_arachidonic acidpost-MI day1
SA387423MI1d_06_arachidonic acidpost-MI day1
SA387424MI1d_07_arachidonic acidpost-MI day1
SA387425MI1d_04post-MI day1
SA387426MI1d_05post-MI day1
SA387427MI1d_02_arachidonic acidpost-MI day1
SA387428MI1d_06post-MI day1
SA387429MI1d_01post-MI day1
SA387430MI1d_02post-MI day1
SA387431MI1d_07post-MI day1
SA387404MI14d_06post-MI day14
SA387405MI14d_04post-MI day14
SA387406MI14d_01_arachidonic acidpost-MI day14
SA387407MI14d_02_arachidonic acidpost-MI day14
SA387408MI14d_03_arachidonic acidpost-MI day14
SA387409MI14d_07post-MI day14
SA387410MI14d_05post-MI day14
SA387411MI14d_03post-MI day14
SA387412MI14d_02post-MI day14
SA387413MI14d_01post-MI day14
SA387414MI14d_04_arachidonic acidpost-MI day14
SA387415MI14d_05_arachidonic acidpost-MI day14
SA387416MI14d_06_arachidonic acidpost-MI day14
SA387417MI14d_07_arachidonic acidpost-MI day14
SA387432MI28d_04_arachidonic acidpost-MI day28
SA387433MI28d_02post-MI day28
SA387434MI28d_03post-MI day28
SA387435MI28d_01_arachidonic acidpost-MI day28
SA387436MI28d_02_arachidonic acidpost-MI day28
SA387437MI28d_03_arachidonic acidpost-MI day28
SA387438MI28d_05_arachidonic acidpost-MI day28
SA387439MI28d_04post-MI day28
SA387440MI28d_05post-MI day28
SA387441MI28d_06post-MI day28
SA387442MI28d_07post-MI day28
SA387443MI28d_06_arachidonic acidpost-MI day28
SA387444MI28d_07_arachidonic acidpost-MI day28
SA387445MI28d_01post-MI day28
SA387446MI7d_05post-MI day7
SA387447MI7d_04post-MI day7
SA387448MI7d_07_arachidonic acidpost-MI day7
SA387449MI7d_06post-MI day7
SA387450MI7d_07post-MI day7
SA387451MI7d_06_arachidonic acidpost-MI day7
SA387452MI7d_05_arachidonic acidpost-MI day7
SA387453MI7d_04_arachidonic acidpost-MI day7
SA387454MI7d_03_arachidonic acidpost-MI day7
SA387455MI7d_02_arachidonic acidpost-MI day7
SA387456MI7d_01_arachidonic acidpost-MI day7
SA387457MI7d_03post-MI day7
SA387458MI7d_01post-MI day7
SA387459MI7d_02post-MI day7
Showing results 1 to 70 of 70

Collection:

Collection ID:CO003656
Collection Summary:Myocardial infarction (MI) was induced in 8-week-old male or female C57BL/6J mice by permanent left anterior descending coronary artery ligation. Mice were then killed by intraperitoneal injection of avertin (30 μl g-1), and cardiac tissue was isolated by saline perfusion through the left ventricle after removal of the right auricle.
Sample Type:Heart

Treatment:

Treatment ID:TR003672
Treatment Summary:Myocardial infarction (MI) was induced in 8-week-old male or female C57BL/6J mice by permanent left anterior descending coronary artery ligation. Mice were then killed by intraperitoneal injection of avertin (30 μl g-1) at 1, 7, 14, and 28 days after infarction, respectively. Cardiac tissue was isolated by saline perfusion of the left ventricle after excision of the right auricle.

Sample Preparation:

Sampleprep ID:SP003670
Sampleprep Summary:A 50-mg sample of mouse heart tissue was extracted using a centrifuge tube with low adsorption properties after adding 1 µl of internal standard mixture. Arachidonic acid (AA) metabolites were extracted with methanol and ethyl acetate under low light conditions. The extracted samples were evaporated to dryness in a gentle stream of nitrogen, after which the samples were dissolved in 30% acetonitrile.

Chromatography:

Chromatography ID:CH004408
Chromatography Summary:Chromatographic separation was performed on an UPLC BEH C18 column (1.7 µm, 50 × 2.1 mm i.d).
Instrument Name:Waters Acquity
Column Name:Waters ACQUITY UPLC BEH C18 (50 x 2.1mm,1.7um)
Column Temperature:40
Flow Gradient:0-1min, 25% B; 1-8min, 25% B-95% B; 8-8.5min, 95% B; 8.5-8.51min, 95% B-25% B; 8.51-9min, 25%B
Flow Rate:0.6mL/min
Solvent A:100% water
Solvent B:100% acetonitrile
Chromatography Type:Reversed phase

Analysis:

Analysis ID:AN005805
Analysis Type:MS
Chromatography ID:CH004408
Num Factors:5
Num Metabolites:72
Units:ng/mL
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