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Impaired angiogenesis in diabetic critical limb ischemia is mediated by a miR-130b-INHBA signaling axis [Human umbilical cells endothelial cells]

ABSTRACT: Impaired angiogenesis in diabetic critical limb ischemia is mediated by a miR-130b-INHBA signaling axis [Human umbilical cells endothelial cells]

PROVIDER: PRJNA841989 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19379104_1.fastq.gz	Fastqsanger.gz
	SRR19379104_2.fastq.gz	Fastqsanger.gz
	SRR19379105_1.fastq.gz	Fastqsanger.gz
	SRR19379105_2.fastq.gz	Fastqsanger.gz
	SRR19379106_1.fastq.gz	Fastqsanger.gz

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Impaired angiogenesis in diabetic critical limb ischemia is mediated by a miR-130b-INHBA signaling axis [Human umbilical cells endothelial cells]

Project description:We report transcriptomic changes in human umbilical vein endothelial cells after transfection of negative control mimic and hsa-miR-130b-3p mimic.

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Impaired angiogenesis in diabetic critical limb ischemia is mediated by a miR-130b-INHBA signaling axis

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Impaired angiogenesis in diabetic critical limb ischemia is mediated by a miR-130b-INHBA signaling axis

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Umbilical Cord Blood-derived Exosomes from Very Preterm Infants with Bronchopulmonary Dysplasia Impaired Endothelial Angiogenesis: Roles of Exosomal MicroRNAs

Project description:Premature infants have a high risk of bronchopulmonary dysplasia (BPD), which is characterized by abnormal development of alveoli and pulmonary vessels. Exosomes and exosomal miRNAs (EXO-miRNAs) from bronchoalveolar lavage fluid are involved in the development of BPD and might serve as predictive biomarkers for BPD. However, the roles of exosomes and EXO-miRNAs from umbilical cord blood of BPD infants in regulating angiogenesis are yet to be elucidated. In this study, we showed that umbilical cord blood-derived exosomes from BPD infants impaired angiogenesis in vitro. Next generation sequencing of EXO-miRNAs from preterm infants without (NBPD group) or with BPD (BPD group) uncovered a total of 418 differentially expressed (DE) EXO-miRNAs. These DE EXO-miRNAs were primarily enriched in cellular function-associated pathways including the PI3K/Akt and angiogenesis- related signaling pathways. Among those EXO-miRNAs which are associated with PI3K/Akt and angiogenesis-related signaling pathways, BPD reduced expression of hsa-miR-103a-3p and hsa-miR-185-5p exhibiting most significant reduction (14.3% and 23.1% of NBPD group, respectively); BPD increased hsa-miR-200a-3p expression by 2.64 folds of NBPD group. Furthermore, overexpression of hsa-miR-103a-3p and hsa-miR-185-5p in normal human umbilical vein endothelial cells (HUVECs) significantly enhanced endothelial cell proliferation, tube formation and cell migration, whereas overexpressing hsa-miR-200a-3p inhibited these cellular responses. This study demonstrates that exosomes derived from umbilical cord blood of BPD infants impair angiogenesis, possibly via DE EXO-miRNAs, which might contribute to the development of BPD.

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