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Differential miRNA expression profiles of human vascular endothelial cells (VECs) between Type-I pro-proliferative/pro-stenotic VECs and Type-II anti-proliferative/anti-stenotic VECs

ABSTRACT: Differential miRNA expression profiles of human vascular endothelial cells (VECs) between Type-I pro-proliferative/pro-stenotic VECs and Type-II anti-proliferative/anti-stenotic VECs

PROVIDER: PRJNA397006 | ENA |

REPOSITORIES: ENA

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Differential miRNA expression profiles of human vascular endothelial cells (VECs) between Type-I pro-proliferative/pro-stenotic VECs and Type-II anti-proliferative/anti-stenotic VECs [Agilent-070156]

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Project description:EPC-derived VECs (EPCdECs) are categorized into two group according to their effects on the proliferation of vascular smooth muscle cells: type-I pro-proliferative VECs and type-II anti-proliferative VECs. Type-II EPCdECs were converted to type-I VECs by repetitive subcultures. Not only subculture-dependent cellular stresses but also donor differences greatly affect the phenotype determination of VECs. By comparing the gene expression profiles of type-II EPCdEC of the first donor (EPC1dEC) at early passage and those of type-II EPC1dEC at late passage and EPCdEC of the second donor at early passage, characteristic gene expression patterns that discriminate Type-I and type-II EPCdECs will be comprehended. Totally three samples of type-I EPC-derived VECs (EPC1dEC[P12], EPC2dEC[P7]) and type-II EPC-derived VEC (EPC1dEC[P7]) were subjected to the analyses.

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Comparison between type-I vascular endothelial cells (VECs) and type-II VECs

Project description:Human VECs are categorized into two groups regarding their effects on the proliferation of vascular smooth muscle cells (VSMCs):type-I, pro-proliferative VECs and type-II anti-proliferative VECs. The effects of VECs on VSMC proliferation were quantitatively assessed according to the following method: human aortic smooth muscle cells, which were stained by PKH-26 in advance, were cultured on the layer of CFSE-stained VECs, and VSMC proliferation were evaluated after four days by flow cytometry analyses using ModFit LTM-bM-^DM-" software (Verity Software House Inc., Topsham, ME). Commercially available primary human VECs including HUVEC, HAEC and HMVEC as well as the majority of endothelial progenitor cell (EPC)-derived VECs (EPCdECs), whether EPCs were obtained from adult or fetal tissues, enhanced VSMC proliferation, showing type-I phenotype. EPCdECs of minor donors including EPC1dEC suppressed VSMC proliferation, showing type-II phenotype. However, type-II VECs turned into type-I VECs after a few rounds of subcultures. Comparative analyses on gene expression profiles between type-I VECs and type-II VECs revealed that regulator of G-protein signaling 5 (RGS5) was the only gene that showed the discriminative expression pattern: high expressions in type-I VECs and low expressions in type-II VECs. Totally six samples of type-I VECs (HUVEC, HAEC, HMVEC, EPC1dEC[P12], UCEPC1dEC, EPC2dEC[P7]) and two samples of type-II VECs (EPC1dEC[P7] and EPC1dEC[P7] purchased at a different time point) were subjected to the analyses.

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Effects of differences in donors and passage numbers of endothelial progenitor cell (EPC)-derived vascular endothelial cells (VECs) on the phenotype determination of VECs (type-I versus type-II).

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