Dataset Information

ELAV proteomics after brain ischemia and reperfusion in the rat

ABSTRACT: We investigated mRNA regulatory proteins of the ELAV family following 10 min global brain ischemia and 8 hrs reperfusion (8R) or non-ischemic controls (NIC) in rat hippocampal CA1 and CA3. There were three main experiments: (1) Shot-gun proteomics of polysome pellets from NIC and 8R CA1 and CA3, (2) Shot-gun proteomics of ELAV immunoprecipitate eluents from NIC and 8R CA1 and CA3, and (3) Proteomics of ELAV antisera-reactive bands excised from nitrocellulose following ELAV Western blot.

OTHER RELATED OMICS DATASETS IN: PRJNA324171

INSTRUMENT(S): QSTAR

ORGANISM(S): Rattus Norvegicus (rat)

TISSUE(S): Brain, Hippocampal Pyramidal Neuron

DISEASE(S): Brain Ischemia

SUBMITTER: Donald DeGracia

LAB HEAD: Donald J. DeGracia

PROVIDER: PXD004078 | Pride | 2016-07-07

REPOSITORIES: Pride

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Publications

Embryonic lethal abnormal vision proteins and adenine and uridine-rich element mRNAs after global cerebral ischemia and reperfusion in the rat.

Wang Haihui H Tri Anggraini Fika F Chen Xuequn X DeGracia Donald J DJ

Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism 20160101 4

Prolonged translation arrest correlates with delayed neuronal death of hippocampal CA1 neurons following global cerebral ischemia and reperfusion. Many previous studies investigated ribosome molecular biology, but mRNA regulatory mechanisms after brain ischemia have been less studied. Here we investigated the embryonic lethal abnormal vision/Hu isoforms HuR, HuB, HuC, and HuD, as well as expression of mRNAs containing adenine and rich uridine elements following global ischemia in rat brain. Prot ...[more]

PMID: 27381823

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Project description:Along with the two hallmark pathologies—intracellular neurofibrillary tangles (NFTs) and extracellular amyloid plaques—transcriptional studies suggest that Alzheimer's disease (AD) results from dysfunction of many cellular pathways including synaptic transmission, cytoskeletal dynamics, and apoptosis. While these studies consistently point to the same pathways involved in AD, there is no consensus on which genes in each pathway are disease-relevant, much less on whether these genes play causative roles or are downstream effects of disease progression. To address these issues, we have performed a large-scale transcriptional analysis in brain of individuals with advanced AD and non-demented controls, focusing specifically on CA1 and the relatively less affected CA3. For comparisons between regions and across disease status, we find consistency in both pathway enrichment as well as specific differentially expressed genes across several studies. Furthermore, genes that show decreased expression with AD progression also tend to show enrichment in CA3 (and vice versa), suggesting that transcription levels in a region may reflect that region's vulnerability to disease. In particular, we find several strong candidate vulnerability (ABCA1, MT1H, PDK4, RHOBTB3) and protection (FAM13A1, LINGO2, UNC13C) genes based on expression patterns. We have also applied weighted gene coexpression network analysis (WGCNA) to explore the pathophysiology of AD from a systems perspective, finding modules for major cell types, which each show distinct disease-relevant expression patterns. In particular, a microglial module shows increased expression in the brain of non-demented controls harboring early NFT pathology, suggesting that microglial activation is an early event in AD progression. Total RNA obtained from 60um sections of frozen human hippocampus was collected using scalpel dissection. Control and AD brains were matched for all non-disease characteristics as closely as possible. CA1 and CA3 dissections for a given individual were taken from the same section. Several region- and disease-related comparisons were performed.

Dataset Information

ELAV proteomics after brain ischemia and reperfusion in the rat

Publications

Embryonic lethal abnormal vision proteins and adenine and uridine-rich element mRNAs after global cerebral ischemia and reperfusion in the rat.

Similar Datasets

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