ArticleStem cell research & therapy2025
MSCs-EXOs containing miR-21a-5p promoted cell proliferation in the rat retinal Müller cell rMC-1 via targeting LATS1.
Article in Stem cell research & therapy, 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.
- Nanoparticle-Mediated Lutein Delivery for Diabetic Retinopathy: From Blood-Retinal Barrier Crossing to Neurovascular Unit Protection.International journal of nanomedicine · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
backgroundDiabetic retinopathy (DR) is a leading cause of blindness in adults, which is characterized by neurovascular dysfunction. Retinal neurodegeneration was involved in the pathogenesis of early-stage DR. This research aims to reveal the therapeutic effects and potential molecule mechanism of Mesenchymal stem cells-derived exosomes (MSCs-EXOs) in Müller cells at the early stage of DR. More specifically, we investigated in the rat retinal Müller cell line rMC-1.
methodsWe cultured rMC-1 in high glucose (HG) medium mixed with MSCs-EXOs to observe the changes in cell proliferative capacity and function. EdU assay, Immunofluorescence staining and Cell viability were used to assess cell proliferative capacity and function. Western blot and Quantitative Real-Time polymerase chain reaction (qRT-PCR) were used to assess the expression of cell proliferation-related proteins and cell cycle-related protein. Finally, dual-luciferase reporter assay, miRNA sequencing and cell transfection were used to assess the relationships between MSCs-EXOs and binding site.
resultsHere our results displayed that MSCs-EXOs promoted HG-induced cell proliferation in rMC-1. Furthermore, MSCs-EXOs protected HG-induced function of rMC-1. Mechanistically, MSCs-EXOs promoted the proliferation of rMC-1 by inhibiting the Hippo pathway to decrease the expression of Large tumor suppressor 1 (LATS1) and p-YAP and increase the expression of cell proliferation-related proteins Yes-associated protein (YAP), EGFR and cell cycle-related protein CYCLIN D1. In addition, LATS1 knockdown inhibited p-YAP expression and promoted HG-induced cell proliferation and YAP, EGFR and CYCLIN D1 expression in rMC-1. We subsequently performed bioinformatics sequencing analysis of MSCs-EXOs and confirmed that LATS1 was the target of miR-21a-5p.
conclusionOur research proved that MSCs-EXOs containing miR-21a-5p increased the expression of YAP via targeting LATS1, and ultimately promoted the cell proliferation in rMC-1. Our current study clarified the molecular mechanism of MSCs-EXOs-regulated cell proliferation and function protection in rMC-1 and provided a novel strategy for the treatment of DR.
Indexed as
Identifiers
What 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.