Lysophosphatidylcholine negatively reverses the effects of human umbilical cord-derived mesenchymal stem cells on high glucose-induced cell dysfunction

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dc.contributor.authorYong Chai
dc.contributor.authorHan Liu
dc.contributor.authorYao Zhao
dc.contributor.authorChunYi Liu
dc.contributor.authorRui Luo
dc.contributor.authorQiang Gan
dc.contributor.authorXian Liu
dc.contributor.departmentBiología Celular e Histología
dc.date.accessioned2025-12-19T11:51:29Z
dc.date.available2025-12-19T11:51:29Z
dc.date.issued2026
dc.description.abstractBackground. Increasing attention has been attracted to the application of human umbilical cord-derived mesenchymal stem cells (HUCMSCs) in the cell therapy of various diabetic complications, including diabetic retinopathy (DR). Lysophosphatidylcholine (LPC) has been reported to induce cell apoptosis and an inflammatory response. The present study aimed to investigate the mechanism of HUCMSCs in high glucose (HG)-treated retinal microvascular endothelial cells (RMECs) and the effect of LPC on this mechanism. Methods. To mimic DR in vitro, RMECs were treated with HG. Flow cytometry analysis was used to identify HUCMSCs and the expression of their surface markers. The apoptosis of RMECs was also accessed using flow cytometry analysis. A CCK-8 assay was performed to measure the viability of RMECs. ELISA was used to detect the concentration of inflammatory cytokines (TNF-α, IL-6, and IL-1β) in RMECs. The protein expression of tight junction proteins in RMECs was examined using western blot analysis. Results. HUCMSCs were identified to present positive markers (CD105, CD73, and CD90) and loss of negative markers (CD45, CD34, and HLA-DR). In RMECs, HG significantly induced a decrease in cell viability and an increase in cell apoptosis and tight junction proteins. Moreover, HG treatment promoted the production of inflammatory cytokines (TNF-α, IL-6, and IL-1β) and facilitated oxidative stress. However, these dysregulated cellular behaviors were alleviated by the treatment of the culture medium of HUCMSCs. Furthermore, LPC treatment reversed the effect of HUCMSCs on HG-induced RMEC injury and impaired the blood-retinal barrier. Moreover, the effect of HUCMSCs on the inflammatory response and oxidative stress of RMEC was also neutralized by LPC treatment. Conclusion. LPC reverses the effects of HUCMSCs on HG-induced RMEC dysfunction, impaired blood-retinal barrier, inflammation, and oxidative stress
dc.formatapplication/pdf
dc.format.extent9
dc.identifier.urihttp://hdl.handle.net/10201/181650
dc.languageeng
dc.publisherUniversidad de Murcia, Departamento de Biologia Celular e Histiologia
dc.relationSin financiacion externa a la Universidad
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 International*
dc.rights.accessRightsinfo:eu-repo/semantics/openAccess
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectLPC
dc.subjectHigh glucose
dc.subjectRMEC
dc.subjectHUCMSCs
dc.subject.odsNo relacionado con ningún objetivo de desarrollo sostenible
dc.titleLysophosphatidylcholine negatively reverses the effects of human umbilical cord-derived mesenchymal stem cells on high glucose-induced cell dysfunction
dc.typeinfo:eu-repo/semantics/article
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Histology and histopathology, Vol.41, Nº1, (2026)