ArticleJournal of molecular medicine (Berlin, Germany)2022
Elucidation of endothelial progenitor cell dysfunction in diabetes by RNA sequencing and constructing lncRNA-miRNA-mRNA competing endogenous RNA network.
Article in Journal of molecular medicine (Berlin, Germany), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Caffeine Sodium Benzoate-Induced Macrophage M1 Polarization Promotes Endothelial Progenitor Cell Dysfunction by Inducing Mitochondrial Dysfunction Via Targeting let-7a-5p/OPA1 Axis.Applied biochemistry and biotechnology · 2026Article
- Endothelial Sestrin2 Coordinates Multiple Protective Pathways to Maintain Angiogenic Function in Diabetes-Associated Endothelial Dysfunction.International journal of molecular sciences · 2025Article
- Endoscopic nasal delivery of engineered endothelial progenitor cell-derived exosomes improves angiogenesis and neurological deficits in rats with intracerebral hemorrhage.Materials today. Bio · 2025Article
- Mogroside V Promotes Osteogenic Differentiation of Bone Marrow Mesenchymal Stem Cells from Diabetic Mice by Altering MicroRNA Profiles.Combinatorial chemistry & high throughput screening · 2025Article
- Identification of genes related to fatty acid metabolism in type 2 diabetes mellitus.Biochemistry and biophysics reports · 2024Article
- Exosomes derived from BMSCs in osteogenic differentiation promote type H blood vessel angiogenesis through miR-150-5p mediated metabolic reprogramming of endothelial cells.Cellular and molecular life sciences : CMLS · 2024Article
- Endothelial progenitor cells as biomarkers of diabetes-related cardiovascular complications.Stem cell research & therapy · 2023Review
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
With the rapid increase in the incidence of diabetes, non-healing diabetic wounds have posed a huge challenge to public health. Endothelial progenitor cell (EPC) has been widely reported to promote wound repairing, while its number and function were suppressed in diabetes. However, the specific mechanisms and competing endogenous RNA (ceRNA) network of EPCs in diabetes remain largely unknown. Thus, the transcriptome analyses were carried in the present study to clarify the mechanism underlying EPCs dysfunction in diabetes. EPCs were successfully isolated from rats. Compared to the control, diabetic rat-derived EPCs displayed impaired proliferation, migration, and tube formation ability. The differentially expressed (DE) RNAs were successfully identified by RNA sequencing in the control and diabetic groups. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses indicated that DE mRNAs were significantly enriched in terms and pathways involved in the functions of EPCs and wound healing. Protein-protein interaction networks revealed critical DE mRNAs in the above groups. Moreover, the whole lncRNA-miRNA-mRNA ceRNA network was constructed, in which 9 lncRNAs, 9 mRNAs, and 5 miRNAs were further validated by quantitative real-time polymerase chain reaction. Rno-miR-10b-5p and Tgfb2 were identified as key regulators of EPCs dysfunction in diabetes. The present research provided novel insight into the underlying mechanism of EPCs dysfunction in diabetes and prompted potential targets to restore the impaired functions, thus accelerating diabetic wound healing. KEY MESSAGES: • Compared to the control, diabetic rat-derived EPCs displayed impaired proliferation, migration, and tube formation ability. • The DE RNAs were successfully identified by RNA sequencing in the control and diabetic groups and analyzed by DE, GO, and KEGG analysis. • PPI and lncRNA-miRNA-mRNA ceRNA networks were constructed. • 9 lncRNAs, 9 mRNAs, and 5 miRNAs were further validated by qRT-PCR. • Rno-miR-10b-5p and Tgfb2 were identified as key regulators of EPCs dysfunction in diabetes.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.