lncRNA‑MIAT facilitates the differentiation of adipose‑derived mesenchymal stem cells into lymphatic endothelial cells via the miR‑495/Prox1 axis.

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

The development of novel treatments for lymphedema is hindered by the poorly understood pathophysiology of the disease. To improve the therapeutic success of treating the disease, the present study aimed to investigate the effects and mechanism of long non‑coding RNA myocardial infarction‑associated transcript (MIAT) in terms of the differentiation of adipose‑derived mesenchymal stem cells (ADMSCs) into lymphatic endothelial cells (LECs). The expression levels of (MIAT), microRNA (miR)‑495 and Prospero‑related homeobox 1 (Prox1) were measured by reverse transcription‑quantitative PCR. The protein expression levels of Prox1, lymphatic vessel endothelial hyaluronan receptor 1 (LYVE‑1), vascular endothelial growth factor receptor‑3 (VEGFR‑3) and podoplanin (PDPL) were detected by western blotting and immunofluorescence. A dual‑luciferase reporter assay was also used to detect the interaction between MIAT, miR‑495 and Prox1. In addition, migration and tube‑formation capabilities were measured by Transwell assay and tube‑formation assay, respectively. The results obtained demonstrated that VEGF‑C156S (recombinant VEGF‑C in which Cys156 was replaced by Ser residue) treatment could efficiently induce the differentiation of ADMSCs into LECs. MIAT expression was upregulated and miR‑495 was downregulated during differentiation. Mechanistically, MIAT upregulated Prox1 expression possibly

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

Browse all related research

Filter the research library by this study's title keywords, author, or publication year.