Background: The purpose of this study was to explore the potential molecular targets of hyperlipidaemia and the related molecular mechanisms.
Methods: The microarray data set of GSE66676 obtained from patients with hyperlipidaemia was downloaded. The weighted gene co‑expression network (WGCNA) analysis was used to analyze the gene expression profile and royalblue module was considered as the highest correlation. Gene Ontology (GO) functional and Kyoto Encyclopedia of Genes and genomes (KEGG) pathway enrichment analyses were implemented for the identification of genes in the royalblue module using the Database for Annotation, Visualization and Integrated Discovery (DAVID) online tool (version 6.8; http://david.abcc.ncifcrf.gov). A protein-protein interaction (PPI) network was established by using the online STRING tool. Then, several hub genes were identified by the MCODE and cytoHubba plug-ins in Cytoscape software.
Results: The significant module (royalblue) identified was associated with TC, TG and Non-HDL-C. GO and KEGG enrichment analyses revealed that the genes in the royalblue module were associated with carbon metabolism, steroid biosynthesis, fatty acid metabolism and biosynthesis of unsaturated fatty acids pathways. SQLE (degree = 17) was revealed as key molecules that associated with hypercholesterolemia (HCH) and SCD was revealed as key molecules that associated with hypertriglyceridemia (HTG). Meanwhile, RT-qPCR analysis also confirmed the above results based on our HCH/HTG samples.
Conclusions: SQLE and SCD are related to hyperlipidaemia, SQLE/SCD may be new targets for cholesterol-lowering or triglyceride-lowering therapy, respectively.
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This is a list of supplementary files associated with this preprint. Click to download.
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On 18 Feb, 2021
On 20 Jan, 2021
Invitations sent on 20 Jan, 2021
On 20 Jan, 2021
On 20 Jan, 2021
Posted 07 Aug, 2020
On 01 Dec, 2020
Received 16 Sep, 2020
On 09 Sep, 2020
Invitations sent on 25 Aug, 2020
On 06 Aug, 2020
On 05 Aug, 2020
On 05 Aug, 2020
On 04 Aug, 2020
On 18 Feb, 2021
On 20 Jan, 2021
Invitations sent on 20 Jan, 2021
On 20 Jan, 2021
On 20 Jan, 2021
Posted 07 Aug, 2020
On 01 Dec, 2020
Received 16 Sep, 2020
On 09 Sep, 2020
Invitations sent on 25 Aug, 2020
On 06 Aug, 2020
On 05 Aug, 2020
On 05 Aug, 2020
On 04 Aug, 2020
Background: The purpose of this study was to explore the potential molecular targets of hyperlipidaemia and the related molecular mechanisms.
Methods: The microarray data set of GSE66676 obtained from patients with hyperlipidaemia was downloaded. The weighted gene co‑expression network (WGCNA) analysis was used to analyze the gene expression profile and royalblue module was considered as the highest correlation. Gene Ontology (GO) functional and Kyoto Encyclopedia of Genes and genomes (KEGG) pathway enrichment analyses were implemented for the identification of genes in the royalblue module using the Database for Annotation, Visualization and Integrated Discovery (DAVID) online tool (version 6.8; http://david.abcc.ncifcrf.gov). A protein-protein interaction (PPI) network was established by using the online STRING tool. Then, several hub genes were identified by the MCODE and cytoHubba plug-ins in Cytoscape software.
Results: The significant module (royalblue) identified was associated with TC, TG and Non-HDL-C. GO and KEGG enrichment analyses revealed that the genes in the royalblue module were associated with carbon metabolism, steroid biosynthesis, fatty acid metabolism and biosynthesis of unsaturated fatty acids pathways. SQLE (degree = 17) was revealed as key molecules that associated with hypercholesterolemia (HCH) and SCD was revealed as key molecules that associated with hypertriglyceridemia (HTG). Meanwhile, RT-qPCR analysis also confirmed the above results based on our HCH/HTG samples.
Conclusions: SQLE and SCD are related to hyperlipidaemia, SQLE/SCD may be new targets for cholesterol-lowering or triglyceride-lowering therapy, respectively.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6
Figure 7
This is a list of supplementary files associated with this preprint. Click to download.
Loading...