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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Genes+Dis
2019 ; 6
(2
): 147-158
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Genome-wide profiling of long noncoding RNA expression patterns and CeRNA
analysis in mouse cortical neurons infected with different strains of borna
disease virus
#MMPMID31193942
Sun L
; Guo Y
; He P
; Xu X
; Zhang X
; Wang H
; Tang T
; Zhou W
; Xu P
; Xie P
Genes Dis
2019[Jun]; 6
(2
): 147-158
PMID31193942
show ga
Borna disease virus 1 (BoDV-1) is neurotropic prototype of Bornaviruses causing
neurological diseases and maintaining persistent infection in brain cells of
mammalian species. Long non-coding RNA (lncRNA) is transcript of more than 200
nucleotides without protein-coding function regulating various biological
processes as proliferation, apoptosis, cell migration and viral infection.
However, regulatory of lncRNAs in BoDV-1 infection remains unknown. To identify
differential expression profiles and predict functions of lncRNA in BoDV-1
infection, microarray data showed that 3528 lncRNAs and 2661 lncRNAs were
differentially expressed in Strain V and Hu-H1 BoDV-infected groups compared with
control groups, respectively. Gene Ontology (GO) and pathway analysis suggested
that differential lncRNAs may be involved in regulation of metabolic, biological
regulation, cellular process, endocytosis, viral infections and cell adhesion
processes, cancer in both BoDV-infected strains. ENSMUST00000128469 was found
down-regulated in both BoDV-infected groups compared with control groups
consistent with microarray (p < 0.05). ceRNA analysis indicated possible
interaction networks as ENSMUST00000128469/miR-22-5p, miR-206-3p, miR-302b-5p,
miR-302c-3p, miR-1a-3p/Igf1. Igf1 was found up-regulated in both BoDV-infected
groups compared with control groups (p < 0.05). Possible functions of predicted
target mRNAs and miRNAs of ENSMUST00000128469 were involved in cell
proliferation, transcriptional misregulation and proteoglycan pathways enriched
in cancer. lncRNA may be involved in regulation of Hu-H1 inhibited cell
proliferation and promoted apoptosis through NF-kB, JNK/MAPK signaling, BCL2 and
CDK6/E2F1 pathways different from Strain V. Possible interaction networks as
ENSMUST00000128469/miR-22-5p, miR-206-3p, miR-302b-5p, miR-302c-3p,
miR-1a-3p/Igf1 may involve in regulation of cell proliferation, apoptosis, and
cancer.