Table 3.
Studies of miRNAs in bipolar disorder.
| MiRNA | Methods | Sample type | Number of samples | Affected function/pathway | |
|---|---|---|---|---|---|
| S. H. Kim et al. (2010), A. H. Kim et al. (2010) | Downregulation: miR-154*, miR-29a, miR-520c-3p, miR-140-3p, miR-767-5p, miR-874, miR-32, miR-573 Upregulation: miR-504, miR-145, miR-145*, miR-22*, miR-133b, miR-154*, miR-889 |
TLDA array | Postmortem tissue - DLPFC (BA46) |
35 BD patients and 35 control subjects |
Using in silico target gene prediction programs, authors reported some predicted genes like tyrosine hydroxylase (TH), phosphogluconate dehydrogenase (PGD) and metabotropic glutamate receptor 3 (GRM3) that are involved in networks overrepresented for neurodevelopment, behavior pathways, and SZ and BP disease development. |
| Moreau et al. (2011) | Downregulation: miR-330, miR-33, miR-193b, miR-545, miR-138, miR-151, miR-210, miR-324-3p, miR-22, miR-425, miR-181a, miR-106b, miR-193a, miR-192, miR-301, miR-27b, miR-148b, miR-338, miR-639, miR-15a, miR-186, miR-99a, miR-190, miR-339 |
Real-time PCR |
Postmortem tissue -PFC |
35 BD patients and 35 control subjects |
Not assessed |
| Miller et al. (2012) | Downregulation, uncorrected p-value: miR-132, miR-132*, miR-150 Upregulation, uncorrected p-value: miR-320, miR-320c, miR-628-3p, miR-874, miR-105, miR-17*, let-7b, let-7f–l* Upregulation, corrected p-value: miR-383, miR-32*, miR-490-5p, miR-196b, miR-513-5p, miR-876-3p, miR-449b, miR-297, miR-188-5p, miR-187 |
Microarray | Postmortem tissue - DLPFC |
31 BD patients and 34 control subjects |
Not assessed |
| Smalheiser et al. (2014) | Downregulation: miR-145-5p, miR-485-5p, miR-370, miR-500a-5p, miR-34a-5p Upregulation: miR-17-5p, miR-579, miR-106b-5p, miR-29c-3p |
TLDA array | Postmortem tissue - PFC (BA10) |
15 BD patients and 15 control subjects |
Not assessed |
| Banigan et al. (2013) | Upregulation: miR-29c | Luminex miRNA expression assay, real-time PCR |
Postmortem tissue - PFC (BA9) - exosomal miRNA |
9 BD patients, 13 control subjects |
Authors emphasized the possible relationship between miR-29c and lithium. miR-29c is induced by canonical Wnt signaling, which is antagonized by GSK-3, a known substrate of inhibition by lithium. |
| Zhu et al. (2009) | No significant alteration in miR-346 | Real-time PCR |
Postmortem tissue - DLPFC (BA 46) |
35 BD patients, 34 controls, 35 SCZ patients |
Not assessed |
| Bavamian et al. (2015) | Upregulation: miR-34a | Real-time PCR |
Postmortem tissue - cerebellar tissue and BD patient-derived neuronal cultures |
29 BD patients, 34 control subjects |
Authors validated two of the putative target genes of miR-34a, Ankyrin-3 (ANK3) and voltage-dependent L-type calcium channel subunit beta-3 (CACNB3), as direct miR-34a targets. |
| Strazisar et al. (2015) | Downregulation: miR-137 | Sanger-based sequencing |
Blood | 345 BD patients, 426 SCZ patients, 1376 control subjects |
Authors’ pathway analysis revealed some pathways that involved in nervous system development and proper synaptic function. |
| Walker et al. (2015) | Upregulation: miR-15b, miR-132 and miR-652 |
TaqMan microRNA assay, real-time PCR |
Blood | 34 unaffected individuals with higher genetic risk of developing a mood disorder, 46 control subjects |
miR-132 is transcribed from a cluster of miRNAs that are known to play an important role in neuronal development and function |
| Rong et al. (2011) | Downregulation: miR-134 | Real-time PCR |
Plasma | 21 BD patients, 21 control subjects |
Authors emphasized the connection between BD and one of the validated miR-134 targets Limk1, that controls synaptic development, maturation and/or plasticity. |