Analyzing differentially expressed genes and pathways of Bex2-deficient mouse lung via RNA-Seq.
Noor BahadarHanif UllahSalah AdlatRajiv Kumar SahMay Zun Zaw MyintZin Mar OoFatoumata Binta BahFarooq Hayel NagiHsu HtooAhmad Ud DinXuechao FengYaowu ZhengPublished in: Turkish journal of biology = Turk biyoloji dergisi (2021)
Bex2 is well known for its role in the nervous system, and is associated with neurological disorders, but its role in the lung's physiology is still not reported. To elucidate the functional role of Bex2 in the lung, we generated a Bex2 knock-out (KO) mouse model using the CRISPR-Cas9 technology and performed transcriptomic analysis. A total of 652 genes were identified as differentially expressed between Bex2 -/- and Bex2 +/+ mice, out of which 500 were downregulated, while 152 were upregulated genes. Among these DEGs, Ucp1, Myh6, Coxa7a1, Myl3, Ryr2, RNaset2b, Npy, Enob1, Krt5, Myl2, Hba-a2, and Nrob2 are the most prominent genes. Myl2, was the most downregulated gene, followed by Npy, Hba-a2, Rnaset2b, nr0b2, Klra8, and Ucp1. Tcte3, Eno1b, Zfp990, and Pcdha9 were the most upregulated DEGs. According to gene enrichment analysis, PPAR pathway, cardiac muscle contraction, and cytokine-cytokine receptor interaction were the most enriched pathways. Besides, the nuclear factor-κB signaling pathway and hematopoietic cell linage pathways were also enriched. Chronic obstructive pulmonary disease (COPD) is enriched among KEGG disease pathways. RT-qPCR assays confirmed the RNA-Seq results. This study opens a new window toward the biological functions of Bex2 in different systems.
Keyphrases
- rna seq
- single cell
- genome wide
- genome wide identification
- chronic obstructive pulmonary disease
- nuclear factor
- crispr cas
- genome wide analysis
- signaling pathway
- mouse model
- dna methylation
- high throughput
- bioinformatics analysis
- transcription factor
- toll like receptor
- lung function
- heart failure
- genome editing
- bone marrow
- epithelial mesenchymal transition
- left ventricular
- cell therapy
- adipose tissue
- pi k akt
- oxidative stress
- gene expression
- wild type