Table 1 Overview of published ECFC transcriptome data
From: Recent advances in endothelial colony-forming cells: from the transcriptomic perspective
Sources | Method | Comparison groups | Available dataset | Main results | Refer-ences |
|---|---|---|---|---|---|
CB-EC-FCs | Single cell sequence | CBMNCs, HUVECs, and CB-ECFC-s | GSE220468 | CB-ECFCs may originate from resident vascular endothelial cells, displaying transcriptome features resembling HUVECs more than any other CBMNC clusters | [43] |
PB-ECF-Cs | RNA sequence | HCAECs, HUVECs, and PB-ECFC-s | GSE131995 | PB-ECFCs express endothelial cell markers of artery, vein, and lymph-vessel, which serve as an intermediate population between HCAECs and HUVECs | [44] |
PB-ECF-Cs | Microarray | ECFCs, AT-ECs and HUVECs | GSE55695 | GO analysis shows that the differences between PB-ECFCs and AT-ECs are within the areas of glycosaminoglycan and heparin binding, vasculature development, extracellular matrix and cell adhesion. The difference between PB-ECFCs and HUVECs is antigen processing and presentation | [45] |
PB-ECF-Cs | RNA sequence | HMECs and PB-ECFC-s | GSE74322 and GSE54416 | GO analysis shows enrichment for the terms “cell adhesion” in HMECs and “single-multicellular organism process” in ECFCs | [46] |
CB-EC-FCs | Small RNA sequencing | CB-ECFC-s and HUVECs | – | CB-ECFCs have lower levels of two anti-angiogenic microRNAs (miR-221 and miR-222) than HUVECs. miR-221-PIK3R1 and miR-222-ETS1 pairs are deregulated in PB-ECFCs from CAD patients | [47] |
PB-ECF-Cs | Single cell sequence | PB-ECFC-s and HUVECs | NCBI dBGaP system: phs002731.v1.p1 | PB-ECFCs exhibit a venous phenotype due to the low expression level of artery markers and high expression of venous markers | [48] |
PB-ECF-Cs | RNA sequence | PB-ECFC-s and lymphatic ECFCs | GSE54416 | Pathway analysis of the top DEGs between PB-ECFCs and lymphatic ECFCs reveals that these DEGs play an important role in regulation of cell differentiation, vasculature development, and endothelial cell differentiation | [46] |
CB-EC-FCs | MiRNA microarray | CB-ECFC-s and PB-ECFC-s | – | miR-193a-3p reduces the angiogenic ability of CB-ECFCs and PB-ECFCs by targeting HMGB1 | [52] |
CB-EC-FCs | Microarray | CB-ECFC-s and PB-ECFC-s | GSM50853-5 GSE20283 | Compared with PB-ECFCs, CB-ECFCs have higher expression of osteogenic and angiogenic genes | [53] |
CB-EC-FCs | Microarray | CB-ECFC-s and PL-ECFCs | – | CB-ECFCs and PL-ECFCs have similar gene expression profiles | [17] |
CB-EC-FCs | MiRNA sequence | Control group and ECFC EVs | – | ECFC EVs deliver miR-21-5p and inhibit THBS1 expression to promote endothelial cell repair | [56] |
PB-ECF-Cs | MiRNA sequence | ECFC and ECFC EVs | – | ECFC EVs ameliorate myocardial infarction by shuttling miR-218-5p/miR-363-3p to modulate the p53/JMY signalling pathway | [57] |
CB-EC-FCs | MiRNA sequence | CB-ECFC-s exosomes and microparticles | – | The transfer of CB-ECFC-EVs with enriched miR-486-5p to the kidney demonstrates protective effects against ischemic kidney injury | [58] |
PB-ECF-Cs | MiRNA sequence | PB-ECFC EVs under normoxic and hypoxic conditions | – | miR-10b-5p is enriched in PB-ECFC EVs under normoxic conditions. PB-ECFC EVs enriched with miR-10b-5p alleviate fibrosis by targeting the fibrotic genes Smurf1 and HDAC4 | [59] |
PB-ECF-Cs | MiRNA microarray | PB-ECFC EVs | – | ECFC EVs with miR-21-5p regulates autophagic flux to promote vascular endothelial repair by inhibiting SIPL1A2 in atherosclerosis | [60] |
CB-EC-FCs | MiRNA sequence | CB-ECFC and ECFC EVs | – | In vivo and in vitro, CB-ECFC EVs promote angiogenesis during ischaemic retinopathy The top five miRNAs enriched in CB-ECFC EVs compared to CB-ECFCs were miR-4532-5p, miR-451a-5p, miR-7704-5p, miR-486–2-5p, and miR-486–1-5p | [61] |
CB-EC-FCs | RNA sequence | hypoxia | GSE142123 | Hypoxia impairs the initial outgrowth of CB-ECFCs and reduces the proliferation of cultured PB-ECFCs Gene expression profiles of PB-ECFCs under hypoxia show the regulation of the cell cycle and metabolism as major altered gene clusters | [63] |
CB-EC-FCs | Microarray | CB-ECFC-s under normoxic oxygen and hypoxic conditions | – | The DEGs of CB-ECFCs under hypoxic conditions are involved in cell apoptosis, cell cycle and MAPK pathways | [64] |
CB-EC-FCs | Microarray | CB-ECFC-s under normoxic and hypoxic conditoins | – | The PLAC8–NOX4 signalling axis improves the angiogenic functions of CB-ECFCs exposed to hypoxia | [65] |
CB-EC-FCs | RNA sequence | ECFCs under normoxic and hypoxic conditions | GSE142123 | ANGPTL14, ENO2, ETXNIP, and SLC2A3 were upregulated while VEGFR2, NOS3, and FLT1 were downregulated. Although the HIF1 pathway is activated, there is no significant enrichment for the VEGFA pathway | [66] |
CB-EC-FCs | Microarray | PT-ECFCs and CT-ECFCs | ArrayExpress database: E-MTAB-4860 | Biogenesis of pro-senescent microparticles by PT-ECFCs is driven by SIRT1-dependent epigenetic regulation of MKK6 | [67] |
CB-EC-FCs | RNA sequence | CB-ECFC-s of lean, overweigh-t and GDM pregnancie-s | GSE228990 | Higher gestational weight gain delays wound healing and reduces expression of long non-coding RNA KLRK1-AS1 in neonatal endothelial progenitor cells | [70] |
CB-ECFCs | Methylation array | ECFCs from healthy women and women with preeclamp-sia | – | DNA methylation of foetal ECFCs is affected in preeclampsia | [75] |
CB-EC-FCs | MiRNA sequence | ECFCs from healthy women and women with preeclamp-sia | – | miR-1270 is downregulated in ECFCs from women with preeclampsia. The downregulation of miR-1270 inhibits tube formation capacity and chemotactic motility | |
CB-EC-FCs | Microarray | ECFCs from healthy pregnancie-s and GDM pregnancie-s | – | Knockdown of PLAC8 improves proliferation and senescence defects of ECFCs from GDM pregnancies | [78] |
PB-ECF-Cs | MiRNA sequence | ECFCs from healthy donors and CAD patients | – | miR-410-3p, miR-497-5p, and miR-2355-5p are upregulated in CAD-ECFCs. Knockdown of these miRNAs can restore the expression of VEGFR2 and increase angiogenic activities of CAD-ECFCs | [82] |
PB-ECF-Cs | MiRNA sequence | ECFCs from healthy donors and CAD patients | – | miR-146a-5p and miR-146b-5p are increased in CAD-ECFCs. miR-146a-5p and miR-146b-5p impair angiogenesis ability by targeting RHOJ | [83] |
PB-ECF-Cs | Microarray | ECFCs from healthy donors and DM patients | GSE43950 | A total of 822 upregulated and 148 downregulated genes are identified as DEGs. IL8 and CXCL1 may lead to the pathophysiology of DM-ECFCs | [86] |
PB-ECF-Cs | Microarray | ECFCs from healthy donors and patients with PDR | – | Two anti-angiogenic genes (TSP1 and TIMP-3) are upregulated in PDR-ECFCs | [87] |
PB-ECF-Cs | MiRNA sequence | ECFCs from healthy donors and patients with IPAH and HPAH | – | Upregulated miR-124 reduces the expression of glycolysis related genes and proliferative abnormalities of PB-ECFCs from PAH | [89] |
PB-ECF-Cs | Microarray | ECFCs from BC and RCC | – | Compared with ECFCs from healthy donors, BC-ECFCs and RCC-ECFCs shared 35 DEGs, 10 of which are organized in a gene network centred on FOS | [93] |
PB-ECF-Cs | Microarray | ECFCs from healthy donors and MDS | – | The frequency and cell adhesion ability of ECFCs are increased in MDS patients. MDS-ECFCs show a hypermethylated phenotype and have a lower expression of several Wnt pathway constituents. The addition of soluble Wnt3A could partially rescue the defects of MDS ECFCs | [95] |
PB-ECF-Cs | MiRNA sequence | ECFCs from control group and type 1 VWD patients | – | ECFC from control group and type 1 VWD patients show DEGs and miRNAs, which may lead to the pathogenesis of type 1 VWD | [97] |
PB-ECF-Cs | Single cell sequence | ECFCs from control group and patients with low VWF levels | NCBI dBGaP system: phs002731.v1.p1 | FLI1 is identified as the candidate gene that mediated the expression level of VWF | [48] |
PB-ECF-Cs | Microarray | ECFCs from control group and patients with uVTE | GSE118259 | The activation of TNFSF15–TNFRSF25 axis reduces survival and proliferation of ECFCs in uVTE patients | [99] |
PB-ECF-Cs | Microarray | ECFCs from control group and patients with MMD | – | RALDH2 is decreased in MMD ECFCs due to defective acetyl-histone H3 binding to the promoter region. Knockdown of RALDH2 in normal ECFCs induces decreased capillary formation in vitro. The panobinostat is a potent therapeutic option for MMD patients | [101] |
PB-ECF-Cs | Microarray | ECFCs from control group and patients with MMD | – | CDKN2A is upregulated in MMD ECFCs. The knockdown of CDKN2A enhances the cell growth and tubule formation ability of MMD ECFCs | [103] |
PB-ECFCs | Microarray | ECFCs from control group and patients with MMD | – | Hypomethylation at the SORT1 promoter CpG sites leads to increased expression of SORT1 in MMD PB-ECFCs. SORT1 overexpression inhibits the tube formation of HUVECs | [104] |