ArticleStem cell reviews and reports2025
TNF-α Pathway Activation and Altered microRNA Expression in Peripheral Blood-Derived Endothelial Colony-Forming Cells: Insights into Diabetes-Induced Dysfunction.
Article in Stem cell reviews and reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
Abstract
backgroundEndothelial colony-forming cells (ECFCs) are progenitors of endothelial cells and have shown angiogenic effects in pre-clinical studies in ischaemic tissues. ECFCs may represent a potential therapy for patients who require vascular repair, including those with diabetes mellitus (DM). However, some, but not all, studies have reported a decrease in the number and impaired function of peripheral blood-derived ECFCs (PB-ECFCs) from patients with diabetes. This study aimed to compare the gene expression profiles and pathways between control and diabetic PB-ECFCs in order to understand mechanisms of diabetes-induced dysfunction.
methodsBulk RNA sequencing (RNA-Seq) was performed to compare the gene expression patterns of PB-ECFCs from control and diabetes groups. Subsequently, gene enrichment analysis (GSEA) was used to identify enriched pathways in PB-ECFCs from the diabetes group. To mimic the inflammatory environment of DM, PB-ECFCs were treated with TNF-α. Changes in gene and microRNA (miRNA) expression following TNF-α exposure were analysed via qRT-PCR. The proliferation, cell adhesion and tube formation ability of PB-ECFCs were assessed using Prestoblue, THP-1 cell adhesion, and in vitro Matrigel assays, respectively.
resultsWe identified 66 differentially expressed genes (28 upregulated and 38 downregulated) between control and diabetic PB-ECFCs. GSEA showed that the TNF-α pathway was markedly enriched in PB-ECFCs from the diabetes group. We then exposed ECFCs to TNF-α and demonstrated activation of inflammatory pathways, which resulted in inhibition of proliferation and potential impairment of tube formation (reducing the number of nodes and total length) in control PB-ECFCs, and enhanced cell adhesion to THP-1. Additionally, we found that three miRNAs (miR-146a-5p, miR-199a-3p, and miR-199a-5p) were upregulated in control PB-ECFCs upon exposure to TNF-α.
conclusionIn summary, this study suggested that the TNF-α pathway may play an important role in the pathophysiology of diabetic PB-ECFCs. The upregulation of miR-146a-5p and miR-199a-3p was likely a compensatory response to the inflammation induced by TNF-α. These findings may provide a rationale for the intervention of intracellular miRNAs as possible targets for improving PB-ECFC function in the inflammatory environment.
Indexed as
Identifiers
40632376What OpenQuestion holds
Registered trials
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 OpenQuestion graph.