Table 1 Evidence of specific functional relationships between vitamin A (including its key derivatives and related compounds) and long noncoding RNAs (lncRNAs)
From: Tracing vitamins on the long non-coding lane of the transcriptome: vitamin regulation of LncRNAs
Vitamin | LncRNA(s) studied in the project | System: Patients / cell line(s) / animal model | Highlighted lncRNA(s)/pathway(s)/target(s)/ partners/ interactions | Disease context/ implication for human disease | Main result(s) | Ref |
|---|---|---|---|---|---|---|
Vitamin A metabolism-associated disorders in pregnancy and early development | ||||||
A | NONRATT021475.2 | Pregnant rats exposed to valproic acid to induce ASD model in offspring. Expression analysis of the lncRNA and mRNA in the hippocampus | NONRATT021475.2/ Desert hedgehog (Dhh) | Autism-Spectrum Disorder | Improvement of valproic acid-induced autism-like behaviors through NONRATT021475.2/Dhh axis | [26] |
Vitamin A and Retinoic Acid (RA) | SULT1C2A | Rat model of vitamin A deficiency (VAD)‐induced Congenital Scoliosis (CS) Human HEK‐293T and H9C2 cells | lncRNA SULT1C2A‐rno‐miR‐466c‐5p‐Foxo4 axis | Congenital Scoliosis | Vitamin A deficiency during pregnancy could induce CS in offspring. Key finding: VAD dysregulated the lncRNA SULT1C2A‐rno‐miR‐466c‐5p‐Foxo4 axis during somitogenesis | [27] |
A | 749 mRNAs, 56 miRNAs, 685 lncRNAs, and 70 circRNAs were differentially expressed | Rat embryos | pathways enriched in VAD-CS pathogenesis: Wnt, PI3K-ATK, FoxO, EGFR, and mTOR | Congenital Scoliosis | In vitamin A deficiency-induced CS, specific lncRNA networks are dysregulated | [28] |
Vitamin A metabolism-associated disorders during adulthood | ||||||
A | high-FCR (H) vs. low-FCR (L): 300 differentially expressed (DE) genes. 40/300 were lncRNAs. 25/40 lncRNAs were significantly correlated with 125 DE protein-coding genes | Yorkshire pig [n = 236, for feed conversion ratio (FCR) assessment] Liver; RN-seq | _ | Pig breeding [Feed efficiency (FE) in pig] | DE genes, including lncRNAs, were enriched in vitamin A, fatty acid, and steroid hormone metabolism pathways | [29] |
Vitamins A (AtRA) and D | LINC00595, SBF2-AS1 (A.fumigatus) and RP11-588G21.2, RP11-394l13.1 (C.albicans detectable in the early phase of infection; CTD3128G10.6 and SRP as potential markers for E. coli infection | Human monocytes Pathogenic fungi: C. albicans (SC5314) & A. fumigatus (AF293) Bacteria: E. coli (isolate 018:K1:H7) | _ | Fungal & bacterial infection | To investigate the roles of vitamins A and D during infection, specific ncRNAs were implicated in infection response MarkersLINC00595, SBF2-AS1 (A.fumigatus), and RP11-588G21.2, RP11-394l13.1 (C.albicans) were detectable in the early phase of infection, hence may be potential therapeutic targets | [30] |
AtRA | Long intergenic noncoding RNA-rat brain expressed (LINC-RBE) | Primary hippocampal neuronal cell culture from adult (16 weeks) male rat (Rattus norvegicus) | _ | Neuronal function | AtRA is involved in transcriptional upregulation of lncRNA expression (here LINC-RBE) | [31] |
AtRA | hTR | human ovarian cancer cell lines | _ | Ovarian carcinoma cells | In AtRA-treated ovarian carcinoma cells, expression of the telomerase components, hTERT and hTR was reduced, implying that ATRA may act by suppressing telomerase activity to inhibit cell growth | [32] |