Evidence map›Paper›PMID 31331330›Full record

ArticleJournal of translational medicine2019

Revealing the pathogenic changes of PAH based on multiomics characteristics.

Li Zhang, Shaokun Chen, Xixi Zeng, Dacen Lin, Yumei Li, Longxin Gui, Mo-Jun Lin

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.1field-weighted citation impact, top 20% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

19 citing papers in PubMed, 34 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Li ZhangDepartment of Physiology & Pathophysiology, Fujian Medical University, Fuzhou, China.
Shaokun ChenDepartment of Physiology & Pathophysiology, Fujian Medical University, Fuzhou, China.
Xixi ZengDepartment of Physiology & Pathophysiology, Fujian Medical University, Fuzhou, China.
Dacen LinDepartment of Physiology & Pathophysiology, Fujian Medical University, Fuzhou, China.
Yumei LiThe Key Laboratory of Fujian Province University on Ion Channel and Signal Transduction in Cardiovascular Disease, School of Basic Medical Sciences, Fujian Medical University, Fuzhou, China.
Longxin GuiThe Key Laboratory of Fujian Province University on Ion Channel and Signal Transduction in Cardiovascular Disease, School of Basic Medical Sciences, Fujian Medical University, Fuzhou, China.
Mo-Jun LinDepartment of Physiology & Pathophysiology, Fujian Medical University, Fuzhou, China. linmojunfj@126.com.
Fujian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPulmonary artery hypertension (PAH), which is characterized by an increase in pulmonary circulation blood pressure, is a fatal disease, and its pathogenesis remains unclear.

methodsIn this study, RNA sequencing (RNA-seq), tandem mass tags (TMT) and reduced representation bisulfite sequencing (RRBS) were performed to detect the levels of mRNA, protein, and DNA methylation in pulmonary arteries (PAs), respectively. To screen the possible pathways and proteins related to PAH, pathway enrichment analysis and protein-protein interaction (PPI) network analysis were performed. For selected genes, differential expression levels were confirmed at both the transcriptional and translational levels by real-time PCR and Western blot analyses, respectively.

resultsA total of 362 differentially expressed genes (|Fold-change| > 1.5 and p < 0.05), 811 differentially expressed proteins (|Fold-change| > 1.2 and p < 0.05) and 76,562 differentially methylated regions (1000 bp slide windows, 500 bp overlap, p < 0.05, and |Fold-change| > 1.2) were identified when the PAH group (n = 15) was compared with the control group (n = 15). Through an integrated analysis of the characteristics of the three omic analyses, a multiomics table was constructed. Additionally, pathway enrichment analysis showed that the differentially expressed proteins were significantly enriched in five Kyoto Encyclopedia of Genes and Genomes (KEGG) biological pathways and ten Gene Ontology (GO) terms for the PAH group compared with the control group. Moreover, protein-protein interaction (PPI) networks were constructed to identify hub genes. Finally, according to the genes identified in the PPI and the protein expression fold-change, nine key genes and their associated proteins were verified by real-time PCR and Western blot analyses, including Col4a1, Itga5, Col2a1, Gstt1, Gstm3, Thbd, Mgst2, Kng1 and Fgg.

conclusionsThis study conducted multiomic characteristic profiling to identify genes that contribute to the hypoxia-induced PAH model, identifying new avenues for basic PAH research.

Indexed as

GenomicsAnimalsDisease Models, AnimalGene Expression RegulationGene Regulatory NetworksHypoxiaMaleProtein Interaction MapsPulmonary Arterial HypertensionRats, Sprague-DawleyReproducibility of ResultsDNA methylationMultiomicsProteomicPulmonary arteriesPulmonary artery hypertensionTranscriptomic

Identifiers

PMID31331330
PMCPMC6647123
OpenAlexW2964046229

What Socratic holds

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LicenceCC BY
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.