Table 3.
Top ten upregulated genes in PAH clusters.
| Cluster | Gene ID | Fold-change | FDR q-value |
|---|---|---|---|
| 2 | TOP2A | 23.31466095 | 3.18E−299 |
| 2 | UBE2C | 20.81621634 | 0 |
| 2 | KIF18A | 20.80020025 | 3.16E−46 |
| 2 | MKI67 | 17.37921703 | 0 |
| 2 | NEK2 | 17.1630725 | 2.83E−84 |
| 2 | PSRC1 | 17.09632113 | 2.95E−71 |
| 2 | NUF2 | 16.73112233 | 1.31E−152 |
| 2 | CKAP2L | 15.91362108 | 4.26E−133 |
| 2 | CENPF | 15.54628052 | 3.5E−316 |
| 2 | SPC25 | 14.05552696 | 4.99E−104 |
| 3 | DTL | 2.864467417 | 1.43E−25 |
| 3 | MCM4 | 2.370515087 | 2.82E−43 |
| 3 | MCM10 | 2.884836554 | 8.37E−26 |
| 3 | TUBA1B | 2.374727347 | 0 |
| 3 | GINS2 | 2.519801484 | 3.60E−63 |
| 3 | CDT1 | 2.22514212 | 5.08E−37 |
| 3 | E2F1 | 2.985704965 | 1.41E−53 |
| 3 | MCM5 | 2.339736103 | 5.60E−47 |
| 5 | TNFSF10 | 3.253200019 | 9.59E−08 |
| 5 | PPP1R16B | 3.177574014 | 5.81E−16 |
| 5 | CSGALNACT1 | 2.985941539 | 1.18E−24 |
| 5 | CXCR4 | 2.983789305 | 3.01E−52 |
| 5 | TM4SF18 | 2.710871286 | 8.57E−18 |
| 5 | RASGRP3 | 2.68766549 | 6.67E−09 |
| 5 | DEPP1 | 2.676648883 | 1.10E−38 |
| 5 | CCL14 | 2.641992743 | 1.25E−05 |
| 5 | RGCC | 2.553964856 | 1.94E−59 |
| 5 | SULF2 | 2.544644983 | 4.64E−30 |
| 6 | CHST1 | 12.52724927 | 3.06E−162 |
| 6 | DEPP1 | 10.92164641 | 2.61E−257 |
| 6 | CXCR4 | 9.002071006 | 9.68E−288 |
| 6 | RASGRP3 | 8.64920468 | 3.82E−69 |
| 6 | VWF | 7.821002651 | 6.27E−191 |
| 6 | PPP1R16B | 7.191421822 | 2.63E−73 |
| 6 | NID2 | 6.666894279 | 3.47E−26 |
| 6 | CSGALNACT1 | 6.174138021 | 2.42E−106 |
| 6 | HOXB5 | 5.980496397 | 4.69E−14 |
| 6 | TNFSF10 | 5.196597822 | 1.09E−26 |
| 7 | PLA2G4C | 3.152371554 | 8.22E−20 |
| 7 | ITGA10 | 3.121176978 | 2.22E−19 |
| 7 | CCL14 | 3.023824847 | 1.09E−06 |
| 7 | FRMD3 | 2.987223157 | 1.90E−13 |
| 7 | AKAP12 | 2.924917691 | 1.01E−52 |
| 7 | CNTNAP3B | 2.845281525 | 3.06E−54 |
| 7 | CDC42EP5 | 2.82167109 | 3.26E−33 |
| 7 | HSPG2 | 2.7813723 | 6.94E−121 |
| 7 | PGF | 2.779502026 | 2.09E−124 |
| 7 | CAMK2N1 | 2.771007913 | 1.09E−19 |
Clusters 1 and 8 in PAH exhibited mostly down-regulated genes. Similar to control cluster 2, PAH cluster 2 overexpressed genes involved in cell proliferation. Interestingly, PAH cluster 3 was also enriched in overexpression of genes involved in cell proliferation (cdt1, DNA replication complex GINS protein (gins2), mcm10, mcm4, and mcm5). PAH cluster 4 did not have any upregulated genes. In cluster 5 contained genes reported in aberrant angiogenesis (ccl14, cxcr4, rasgrp3 and Extracellular sulfatase Sulf-2 (sulf2)). Similar to control cluster 6, PAH cluster 6 was enriched in genes regulating immune cell—endothelial interaction and new vessel formation. Genes upregulated in PAH cluster 7 were compatible with an angiogenic phenotype (A-Kinase Anchoring Protein 12 (akap12); ccl14; pgf and Cell Division Cycle 42 Pseudogene 5 (cdc42p5)).