Dataset Information

Time-series proteome profiling analysis of the atria in a murine model of angiotensin II-induced atrial fibrillation

ABSTRACT: Atrial fibrillation (AF) is the most common form of arrhythmia observed in clinical cardiac diseases. Angiotensin II (Ang II) and elevation of blood pressure have been considered to be the main risk regulators of AF. However, the time series proteome profiling and the key signaling pathways involved in the development of Ang II-induced AF remain unclear. Wild-type C57BL/6 male mice (10 weeks old) were infused with Ang II (2000 ng/kg/min) for 1, 2 and 3 weeks, respectively. AF inducibility, left atrial volume and fibrosis were examined by echocardiography and histological staining. The time series proteome in atria tissues was evaluated with Isobaric tags for relative and absolute quantitation (iTRAQ) and liquid chromatography coupled with tandem mass spectrometry (LC-MS/MS) technologies. This study defined the dynamic changes of the differentially expressed proteins (DEPs) involved in Ang II-induced AF, and identified that mitochondrial oxidative phosphorylation may play a key role in this disease. These findings provide a resource for understanding the molecular mechanism research of AF.

INSTRUMENT(S): Q Exactive Plus

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Atrium

SUBMITTER: Yun-Long Zhang

LAB HEAD: Hui Hua Li

PROVIDER: PXD022238 | Pride | 2022-04-04

REPOSITORIES: Pride

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Time series proteome profile analysis reveals a protective role of citrate synthase in angiotensin II-induced atrial fibrillation.

Teng Fei F Han Xiao X Yu Peng P Li Pang-Bo PB Li Hui-Hua HH Zhang Yun-Long YL

Journal of hypertension 20220401 4

<h4>Background</h4>Angiotensin (Ang) II and elevated blood pressure are considered to be the main risk factors for atrial fibrillation. However, the proteome profiles and key mediators/signaling pathways involved in the development of Ang II-induced atrial fibrillation remain unclear.<h4>Methods</h4>Male wild-type C57BL/6 mice (10-week old) were infused with Ang II (2000 ng/kg per min) for 1, 2, or 3 weeks, respectively. Time series proteome profiling of atrial tissues was performed using isobar ...[more]

PMID: 35013064

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Project description:Gliomas are aggressive primary brain tumors, presenting surgery limitations due to their highly infiltrative potential. The expression of Angiotensin II (Ang II) receptors in human astrocytomas was previously associated with a poor prognosis. Accordingly, this study was undertaken to reveal the molecular mechanisms underlying Ang II actions in gliomas through the transcriptomic analysis of glioma cells exposed to Ang II. C6 glioma cells were treated with Ang II and specific antagonists of AT1 and AT2. Total RNA was isolated at three and six hours intervals and submitted to oligonucleotide microarray protocol. The differentially expressed genes were obtained by paired t-tests with p<0.05 and interpreted using Venn diagrams, functional enrichment and protein interaction network analyses. Validation of microarray results was carried out through qPCR experiments of selected genes. We found a high number of significant genes with low fold changes in gene expression at the time intervals studied. These genes were regulated in a time dependent-manner, with most gene expression changes being exclusive to one of the time intervals evaluated. Our results indicated that blocking AT1 or AT2 changed the expression of genes involved in regulation of transcription, cell cycle, cell proliferation, differentiation, apoptosis, cell adhesion, cell migration, regulation of actin cytoskeleton, protein transport and protein ubiquitination. Additionally, the signaling pathways over-represented by the significant genes were ErbB, mTOR, MAPK, neurotrophin, insulin and Wnt. Finally, interactome analyses revealed hub genes associated with cell proliferation, survival, migration, transport, structural support, neurotrophin pathway, MAPK signaling and Wnt signaling. Taken together, our findings implicate Ang II-transcriptional regulation in glioma progression by means of the modulation of genes participating in protumoral functions. This transcriptome pattern is observed upon Ang II activation of either AT1 or AT2 receptors, thereby highlighting the relevance of both receptor subtypes in glioma progression. Interactome analyses disclosed hub genes regulated by Ang II which may present higher control over their networks. These genes participate in biological functions that could enhance the degree of malignancy in gliomas and thus should be further explored. C6 cells were cultured in Dulbecco's modified Eagle's medium (DMEM) supplemented with 10% fetal bovine serum, 100 Units/ml penicillin and 100 M-BM-5g/ml streptomycin. Cells were seeded in cell culture dishes and incubated at 37M-BM-0C/ 5% CO2 until becoming confluent. Then, these cells were pre-treated (30 minutes) with either AT1 receptor antagonist (Losartan: 10-5M) or AT2 receptor antagonist (PD123319: 10-5M) followed by Ang II treatment (10-7 M) according to the treatment scheme: Group 1 M-bM-^@M-^S control; Group 2 M-bM-^@M-^S cells only treated with Ang II; Group 3 M-bM-^@M-^S cells pre-treated (30 minutes) with Losartan and then treated with Ang II; Group 4 M-bM-^@M-^S cells pre-treated (30 minutes) with PD123319 and then treated with Ang II. To identify which genes were significantly differentially expressed, paired t-tests (p<0.05) were performed in the following comparisons: Ang II x Control (3h); Ang II x Control (6h); Ang II +Los x Ang II (3h); Ang II +Los x Ang II (6h); Ang II +PD123319 x Ang II (3h); Ang II +PD123319 x Ang II (6h).

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