RGD Reference Report - Quantitative proteomic analysis of intracerebral hemorrhage in rats with a focus on brain energy metabolism. - Rat Genome Database

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Quantitative proteomic analysis of intracerebral hemorrhage in rats with a focus on brain energy metabolism.

Authors: Liu, Tao  Zhou, Jing  Cui, Hanjin  Li, Pengfei  Li, Haigang  Wang, Yang  Tang, Tao 
Citation: Liu T, etal., Brain Behav. 2018 Nov;8(11):e01130. doi: 10.1002/brb3.1130. Epub 2018 Oct 11.
RGD ID: 408426007
Pubmed: PMID:30307711   (View Abstract at PubMed)
PMCID: PMC6236229   (View Article at PubMed Central)
DOI: DOI:10.1002/brb3.1130   (Journal Full-text)


INTRODUCTION: Intracerebral hemorrhage (ICH) is a lethal cerebrovascular disorder with a high mortality and morbidity. The pathophysiological mechanisms underlying ICH-induced secondary injury remain unclear.
METHODS: To examine one of the gaps in the knowledge about ICH pathological mechanisms, isobaric tag for relative and absolute quantification (iTRAQ)-based liquid chromatography-tandem mass spectrometry (LC-MS/MS) was used in collagenase-induced ICH rats on the 2nd day.
RESULTS: A total of 6,456 proteins were identified with a 1% false discovery rate (FDR). Of these proteins, 126 and 75 differentially expressed proteins (DEPs) were substantially increased and decreased, respectively. Based on Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and STRING analyses, the protein changes in cerebral hemorrhage were comprehensively evaluated, and the energy metabolism in ICH was anchored. The core position of the nitrogen metabolism pathway in brain metabolism in ICH was found for the first time. Carbonic anhydrase 1 (Ca1), carbonic anhydrase 2 (Ca2), and glutamine synthetase (Glul) participated in this pathway. We constructed the protein-protein interaction (PPI) networks for the energy metabolism of ICH, including the Atp6v1a-Atp6v0c-Atp6v0d1-Ppa2-Atp6ap2 network.
CONCLUSIONS: It seems that dysregulation of energy metabolism, especially nitrogen metabolism, may be a major cause in secondary ICH injury. This information provides novel insights into secondary events following ICH.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
ATP6V1AHumanCerebral Hemorrhage  ISOAtp6v1a (Rattus norvegicus)protein:decreased expression:brainRGD 
Atp6v1aRatCerebral Hemorrhage  IEP protein:decreased expression:brainRGD 
Atp6v1aMouseCerebral Hemorrhage  ISOAtp6v1a (Rattus norvegicus)protein:decreased expression:brainRGD 
CA2HumanCerebral Hemorrhage  ISOCar2 (Rattus norvegicus)protein:increased expression:brainRGD 
Car2RatCerebral Hemorrhage  IEP protein:increased expression:brainRGD 
Car2MouseCerebral Hemorrhage  ISOCar2 (Rattus norvegicus)protein:increased expression:brainRGD 

Objects Annotated

Genes (Rattus norvegicus)
Atp6v1a  (ATPase H+ transporting V1 subunit A)
Car2  (carbonic anhydrase 2)

Genes (Mus musculus)
Atp6v1a  (ATPase, H+ transporting, lysosomal V1 subunit A)
Car2  (carbonic anhydrase 2)

Genes (Homo sapiens)
ATP6V1A  (ATPase H+ transporting V1 subunit A)
CA2  (carbonic anhydrase 2)


Additional Information