Human umbilical cord mesenchymal stem cells pretreated with Angiotensin-II attenuate pancreas injury of rats with severe acute pancreatitis - 31/07/19
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| Iconographies | 9 |
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| Autres | 0 |
Highlights |
• | Ang-II has been reported to be involved in key events of the inflammatory process and tissue damage. |
• | Cell-based therapy has been proved to be effective in the treatment SAP. |
• | Pretreatment is the adaptation of MSCs to Ang-II in advance to mitigate endogenous Ang-II damage. |
• | Ang-II is a good trigger for pretreating MSCs to enhance the paracrine release of growth factors (GFs). |
• | Ang-II-MSCs can increase paracrine production of VEGF, improved the anti-apoptosis capacity of endothelial cells. |
Abstract |
Mesenchymal stem cells (MSCs) pretreatment is an effective route for improving cell-based therapy of endothelial cell survival, vascular stabilization, and angiogenesis. We hypothesized that the application of human umbilical cord-MSCs (hUC-MSCs) pretreated with angiotensin-II (Ang-II) might be a potential therapeutic approach for severe acute pancreatitis (SAP). Therefore, the effect of Ang-II pretreated hUC-MSCs on SAP was investigated in vitro and in vivo.
Methods |
In the present study, human umbilical cord-derived MSCs pretreated with or without Ang-II were delivered through the tail vein of rats 12 h after induction of SAP. Pancreatitis severity scores and serum lipase levels, as well as the levels of VEGF and VEGFR2 were evaluated.
Results |
We found that the administration of Ang-II-MSCs significantly inhibited pancreatic injury, as reflected by reductions of pancreatitis severity scores, serum amylase and serum lipase levels. Furthermore, the reduced apoptotic rate and increased tube formation in human umbilical vein endothelial Cells (HUVEC) were found resulting from the administration of Ang-II-MSC-CM. Moreover, knockdown of VEGFR2 can block the effect of Ang-II-MSC-CM on preventing HUVEC from apoptosis, as well as the capacity of tube formation was also suppressed. In addition, the expression of increased Bcl-2 and alleviated caspase-3 were observed in HUVEC and HUVEC transfectants exposure to Ang-II-MSC-CM.
Conclusion |
Collectively, these results elucidated that the pretreatment of hUC-MSCs with Ang-II improved the outcome of MSC-based therapy for SAP via enhancing angiogenesis and ameliorating endothelial cell dysfunction in a VEGFR2 dependent manner.
Le texte complet de cet article est disponible en PDF.Keywords : Angiotensin-II, hUC-MSCs, SAP, Angiogenesis, Endothelial cells
Plan
Vol 117
Article 109052- septembre 2019 Retour au numéro
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