RNA sequencing data describing transcriptional changes in aorta of ApoE-/- mice after alpha 7 nicotinic acetylcholine receptor (α7nAChR) stimulation

This manuscript is a companion paper to Ulleryd M.U. et al., “Stimulation of alpha 7 nicotinic acetylcholine receptor (α7nAChR) inhibits atherosclerosis via immunomodulatory effects on myeloid cells” Atherosclerosis, 2019 [1]. Data shown here include RNA sequencing data from whole aorta of ApoE-/- mice fed high fat diet and treated with the alpha 7 nicotinic acetylcholine receptor (α7nAChR) agonist AZ6983 for 8 weeks using subcutaneously implanted osmotic minipumps. Here we present the top gene networks affected by treatment with AZ6983, as well as the up- and down-regulated genes in aorta after treatment. Further, a URL link to the RNA sequencing datasets submitted to GEO is included.

. Data shown here include RNA sequencing data from whole aorta of ApoE-/-mice fed high fat diet and treated with the alpha 7 nicotinic acetylcholine receptor ( α7nAChR) agonist AZ6983 for 8 weeks using subcutaneously implanted osmotic minipumps. Here we present the top gene networks affected by treatment with AZ6983, as well as the up-and down-regulated genes in aorta after treatment. Further, a URL link to the RNA sequencing datasets submitted to GEO is included.

Value of the data
• These data provide information on the transcriptional effects on whole aorta after treatment with alpha 7 nicotinic acetylcholine receptor ( α7nAChR) agonist AZ6983 in the atherosclerosis-prone ApoE-/-mouse.
• Researchers interested in atherosclerosis, as well as, α7nAChR signaling will find these data a valuable resource.
• The information provided here may be used for future studies on how α7nAChR stimulation influence the vascular transcriptome.
• These data can generate hypothesis for new studies investigating the α7nAChR-related transcriptomic profiles, as well as signaling pathways, in other tissues • The present data on α7nAChR signaling is predominantly available from cell culture experiments, using cell lines, this data set provides additional information on the signaling pathways in tissue from long-term treatment in vivo.

Data description
To investigate the effects of alpha 7 nicotinic acetylcholine receptor ( α7nAChR) stimulation on atherosclerosis in apolipoprotein E deficient (ApoE-/-) mice, mice were treated with α7nAChR agonist AZ6983 for 8 weeks. Thoracic aortas were used for RNA sequencing analysis. Fig. 1 describes the top two networks identified with Ingenuity Pathway Analysis (IPA) software for differently expressed genes in aorta of ApoE-/-mice treated with AZ6983 compared with controls. Major functions of the networks are indicated in A and B, followed by the network score. Networks are ranked according to their degree of relevance to the eligible network molecules in the data set and the score is calculated with an algorithm based on p-scores derived from q-values. Table 1 shows the complete list of up-and down-regulated genes in the aorta after treatment with AZ6983 ranked by q-value.

Experimental animals
Male apoE-/-mice (C57BL/6 background, B6192P2-Apoetm1UncN11, Taconic, Denmark) were kept at the Laboratory for Experimental Biomedicine, Gothenburg, Sweden. At 10 weeks of age, mice were anesthetized using isoflurane and subcutaneously implanted with osmotic minipumps Table 1 Complete list of up-and down-regulated genes in the aorta after treatment with AZ6983, ranked by q-value.

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RNA isolation, RNA sequencing and ingenuity pathway analysis
RNA of thoracic aorta was extracted by using the RNAeasy R Fibrous Tissue Mini Kit (Qiagen GmbH, Hilden, Germany) according to the manufacturer's protocol. Concentration and quality was analyzed using a NanoDrop (NanoDrop Products, DE, US) and electrophoresis (Experion, Bio-Rad Laboratories, CA, USA).
Aortic RNA from mice treated with AZ6983 (n = 6) or controls (n = 6) was isolated as described above and Stranded Total RNA Sample preparations were performed using the Illumina True-Seq Stranded Total RNA Sample Preparation Kit with Ribo Sero Gold according to the TruSeq Stranded Total RNA Sample Preparation Guide (15031048 Rev. E). Sequencing of the enriched libraries was performed on Illumina Nextseq500 (2x75bp). The quality of the data was analyzed with FastQC and reads with an average quality score of > 30 were included in the sequencing. Differentially expressed genes (DEGs) were identified using the DESeq2-method with Benjamini Hochberg adjusted p-values (q-values) [2] and a FDR-q of 10%.
QIAGEN's Ingenuity R Pathway Analysis (IPA R , QIAGEN Redwood City, content version 42012434) was used to study potential functions of AZ6983 treatment in the aorta [3][4][5] . Network analysis was generated by overlaying the eligible network molecules in the data set with the global gene network contained in the Ingenuity R Knowledge Base. Networks are ranked according to their degree of relevance to the genes in the data set. Functional analysis identified the top ranked biological functions and diseases that were enriched in the dataset by calculating the number of molecules that cohere to a functional category and was estimated by Fisher's exact test (q < 0.05). Activation Z-score predicts if a specific function is activated ( ≥ 2) or inhibited ( ≤ −2) and is supported by one or more references from Ingenuity R Knowledge Base.
Top two networks identified with Ingenuity Pathway Analysis (IPA) software for genes that were differently expressed in aorta of ApoE -/mice treated with AZ6983 compared with controls. Major functions of the networks are indicated in A and B, followed by the network score. Networks are ranked according to their degree of relevance to the eligible network molecules in the data set and the score is calculated with an algorithm based on p-scores derived from qvalues. The up-(red) or down-(green) regulation of genes are indicated by the intensity of node color, and the functional class of the gene product is indicated by different symbols. Relationship between genes are supported by one or more references and illustrated with a connecting line.
Wera Cornells foundation, Dr. Felix Neuberghs Foundation, Emelle Foundation, Mary von Sydow foundation, Wilhelm and Martina Lundgren foundation and grants from the Swedish state under the agreement between the Swedish government and the county councils, the ALF-agreement (ALF GBG-723131).

Supplementary materials
Supplementary material associated with this article can be found, in the online version, at doi: 10.1016/j.dib.2020.105415 .