Expression profiling of Nme7 interactome in experimental models of metabolic syndrome

Title:

Expression profiling of Nme7 interactome in experimental models of metabolic syndrome

Creator:

Lucie Šedová, Školníková, E, Hodúlová, M, Josef Včelák, Ondřej Šeda, and Běla Bendlová

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:701a6c6e-6761-4060-a9b7-bed75116804f
uuid:701a6c6e-6761-4060-a9b7-bed75116804f
issn:0862-8408

Subject:

Fyziologie člověka a srovnávací fyziologie, syndrom inzulinové rezistence, insulin resistance syndrome, metabolic syndrome, transcriptomics, recombinant inbred strains, ciliopathy, 14, and 612

Type:

model:article and TEXT

Format:

print, bez média, and svazek

Description:

Nucleoside diphosphate kinase 7, non-metastatic cells 7 (NME7) is an acknowledged member of ciliome and is involved in the biogenesis or function of cilia. As obesity and diabetes are common in several ciliopathies, we aimed to analyze changes of gene expression within Nme7 interactome in genetically designed rat models of metabolic syndrome. We assessed the liver transcriptome by Affymetrix microarrays in adult males of 14 PXO recombinant inbred rat strains and their two progenitor strains, SHR-Lx and BXH2. In the strains with the lowest expression of Nme7, we have identified significant enrichment of transcripts belonging to Nme7 interactome. In the subsequent network analysis, we have identified three major upstream regulators - Hnf4a , Ppara and Nr1h4 and liver steatosis (p=0.0001) and liver necrosis/cell death (apoptosis of liver cells, p=0.0003) among the most enriched Tox categories. The mechanistic network reaching the top score showed substantial overlap with Assembly of non-motile cilium and Glucose metabolism disorder gene lists. In summary, we show in a genetic model of metabolic syndrome that rat strains with the lowest expression of Nme7 present gene expression shifts of Nme7 interactome that are perturbing networks relevant for carbohydrate and lipid metabolism as well as ciliogenesis., L. Šedová, E. Školníková, M. Hodúlová, J. Včelák, O. Šeda, B. Bendlová., and Obsahuje bibliografii

Language:

English

Rights:

http://creativecommons.org/publicdomain/mark/1.0/
policy:public

Source:

Physiological research | 2018 Volume:67 | Number:Suppl 3

Harvested from:

CDK

Metadata only:

false