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Effect of mir-210-3p on The Function of c-kit+ Cardiac Progenitor Cells under Ischemia and Hypoxia

ABSTRACT: Effect of mir-210-3p on The Function of c-kit+ Cardiac Progenitor Cells under Ischemia and Hypoxia

PROVIDER: PRJNA956826 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24203211.fastq.gz	Fastqsanger.gz
	SRR24203212.fastq.gz	Fastqsanger.gz
	SRR24203213.fastq.gz	Fastqsanger.gz
	SRR24203214.fastq.gz	Fastqsanger.gz
	SRR24203215.fastq.gz	Fastqsanger.gz

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Similar Datasets

Effect of mir-210-3p on The Function of c-kit+ Cardiac Progenitor Cells under Ischemia and Hypoxia

Project description:C-kit+ cardiac progenitor cells (CPCs) play an important role in improving the prognosis of ischemic heart disease. MicroRNAs have been shown to have a protective role in the cardiac repair process, but their specific functional mechanisms are still unclear. The aim of this study was to screen for differentially expressed miRNAs in c-kit+ CPCs under hypoxia and explore their effects on the function of c-kit+ CPCs. We found that miR-210-3p was significantly upregulated in hypoxia-treated c-kit+ CPCs through second-generation sequencing. Protein chip detection revealed that c-kit+ CPCs could express cytokines such as FGF basic, Angiogenin, and VEGF, and that hypoxia could enhance the secretion of some angiogenesis-related factors. Silencing miR-210-3p, on the other hand, resulted in a reduction in the secretion of these angiogenesis-related factors. In addition, we found that the conditioned medium of hypoxia-treated c-kit+ CPCs could promote the proliferation, migration, and tube formation ability of mouse cardiac microvascular endothelial cells (CMECs). Conversely, the conditioned medium of c-kit+ CPCs with silenced miR-210-3p after hypoxia inhibited the proliferation, migration, and tube formation ability of CMECs. These results suggest that c-kit+ CPCs may exert their pro-angiogenic effects through paracrine mechanisms, which are regulated by miR-210-3p. The upregulation of miR-210-3p in hypoxia-treated c-kit+ CPCs may enhance their paracrine function by regulating the secretion of angiogenic factors, thereby promoting angiogenesis in ischemic heart disease. Therefore, miR-210-3p plays a key role in regulating the paracrine function of c-kit+ CPCs and can affect the process of angiogenesis. The role of miR-210-3p has potential application value for the treatment of ischemic heart disease, and may become one of the important targets for future treatment of ischemic heart disease.

2023-08-16 | GSE229934 | GEO

Hypoxia-induced miR-210 modulates gene expression in response to acute peripheral ischemia.

Project description:Peripheral Artery Disease is caused by the restriction or occlusion of arteries supplying the leg. Better understanding of the molecular mechanisms underpinning tissue response to acute and chronic ischemia is urgently needed to improve therapeutic options. The aim of this study is understanding miR-210 regulation and role in a mouse model of hindlimb ischemia. To investigate miR-210 function, mice were injected with a miR-210 complementary LNA-oligonucleotide (anti-miR-210). Then, the left femoral artery was dissected in order to induce unilateral hindlimb ischemia. Mice were sacrified 3 days later and gene expression profiles of gastrocnemius muscles were obatained.

2015-10-23 | E-GEOD-43340 | biostudies-arrayexpress

Hypoxia-induced miR-210 modulates gene expression in response to acute peripheral ischemia.

2015-10-23 | GSE43340 | GEO

Effect of overexpression of miR-210-3p on gene expression of human umbilical vein endothelial cells in hypoxic conditions

Project description:To investigate machanism of miR-210-3p regulating angiogenic ability of human umbilical vein endothelial cells (HUVECs) in hypoxic conditions, we transfected miR-210-3p mimic to overexpress miR-210-3p in human umbilical vein endothelial cells. We than performed RNA sequencing of miR-210-3p mimic-transfected and control HUVECs under hypoxic conditions to evaluate the transcriptional changes in the miR-210-3p-overexpressing HUVECs.

2022-09-28 | GSE214170 | GEO

miR-210 expression is strongly hypoxia-induced in anaplastic thyroid cancer cell SW1736

Project description:Anaplastic thyroid carcinoma (ATC) is a rare but deadly form of thyroid cancer. Hypoxia is frequent in aggressive solid tumors like ATC and can promote resistance to therapy via the hypoxia-inducible factor (HIF) pathway. miR-210 has been previously identified as a direct target of hypoxia-inducible factor 1 (HIF-1) and is upregulated in many solid tumors. Here we show that miR-210 expression is upregulated in ATC cell line SW136 in hypoxia relative to normoxia. Identifying and targeting hypoxic cells is an attractive approach to detecting and treating ATC.

2022-09-08 | GSE212703 | GEO

Transcription profiling of rat NRVMs response to ischemia and reperfusion events using Coverslip Hypoxia

Project description:NRVMs were subjected to varying durations of ischemia or ischemia+reperfusion using coverslip hypoxia. Expression profiling was used to identify genes that are differentially regulated in either event. We used microarrays to detail the global program of gene expression underlying ischemia and reperfusion using Coverslip Hypoxia and identified distinct classes of genes regulated during these processes. Experiment Overall Design: RNA was extracted from NRVMs subjected to varying durations of ischemia or ischemia+reperfusion and hybridized to rat genome Affymetrix arrays.

2008-06-15 | E-GEOD-6701 | biostudies-arrayexpress

Expression data from ischemia and reperfusion events in NRVMs using Coverslip Hypoxia

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Identification of miR-210 target genes in T20 patient-derived sphere culture

Project description:Hypoxia is known to regulate tumor-initiating cells and to have an effect on miRNA expression. We were interested in studying the role of hypoxia-induced miR-210 in colorectal cancer patient-derived sphere cultures. Downregulated genes after overexpression of miR-210 were retained as potential miR-210 target genes for further validation sudies.

2016-10-27 | GSE80236 | GEO

Paracrine effects of mir-210-3p on angiogenesis in hypoxia-treated c-kit-positive cardiac cells.

Project description:Objective: Treatment with c-kit-positive cardiac cells (CPCs) has been shown to improve the prognosis of ischemic heart disease. MicroRNAs (miRNAs) confer protection by enhancing the cardiac repair process, but their specific functional mechanisms remain unclear. This study aimed to screen for differentially expressed miRNAs in CPCs under hypoxia and explore their effects on the function of CPCs.Methods: We harvested CPCs from C57 adult mice and later performed a high-throughput miRNA sequencing for differential expression profiling analysis. Subsequently, we intervened with the differentially expressed gene miR-210-3p in CPCs and detected changes in the secretion of angiogenesis-related factors through a protein-chip analysis. Finally, we applied CPC supernatants of different groups as conditioned medium to treat mouse cardiac microvascular endothelial cells (CMECs) and further investigated the functional effects of miR-210-3p on c-kit+CPCs under ischemia and hypoxia conditions.Results: The miR-210-3p was highly increased in hypoxia-treated CPCs. Protein-chip detection revealed that CPCs expressed cytokines such as FGF basic, angiogenin, and vascular endothelial growth factor (VEGF) and that hypoxia enhanced their release. Silencing miR-210-3p resulted in a reduction in the release of these angiogenesis-related factors. In addition, the conditioned medium of hypoxia-treated CPCs promoted the proliferation, migration, and tube-forming capabilities of CMECs. In contrast, the conditioned media of CPCs with silenced miR-210-3p after hypoxia decreased the proliferation, migration, and tube-forming ability of CMEC.Conclusions: The CPCs exert proangiogenic effects via paracrine pathways mediated by miR-210-3p. Upregulation of miR-210-3p in hypoxia-treated CPCs may enhance their paracrine function by regulating the secretion of angiogenic factors, thereby promoting angiogenesis in ischemic heart disease.

| S-EPMC10364570 | biostudies-literature

MiR-210 impact on the transcriptome suggests regulation of inflammation and regeneration pathways

Project description:In order to understand the consequences of miR-210 blocking on the ischemia response, the transcriptomic changes were investigated by microarray technology in gastrocnemius muscles of ANTI-210 and SCR treated mice, 7 days after ischemia. Identified differentially expressed genes were used to perform gene-ontology enrichment-analysis, allowing to identify several terms falling into the biological macro areas of angiogenesis and blood vessel development, as well as related categories, such as cell adhesion, migration and proliferation. These findings are in agreement with the identified positive role played by miR-210 in the neo-vascularization process. Furthermore, many terms were also related to metabolism and mitochondrial organization, in keeping with the role of miR-210 in the regulation of oxidative phosphorylation.

2020-02-05 | GSE142262 | GEO

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