Liraglutide Enhances the Efficacy of Human Mesenchymal Stem Cells in Preserving Islet ß-cell Function in Severe Non-obese Diabetic Mice

Li, Lirong; Lu, Junyan; Jia, Xiaolei; Hui, Hui; Zhang, Jie; Liu, Ying; Cui, Weijuan; Xu, Qianyue; Zhu, Dalong

doi:10.2119/molmed.2016.00168

Cited by 9 publications

(5 citation statements)

References 33 publications

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“…Therefore, we investigated the effect of LIRA on the proliferation and migration of hPDLCs. LIRA can promote proliferation of various cells, including pancreatic β‐cells, endothelial cells, bone marrow mesenchymal cells, as well as osteoblasts . In this study, MTT assay data showed that LIRA promoted the proliferation of hPDLCs in a concentration‐dependent manner.…”

Section: Discussionsupporting

confidence: 48%

The effect of liraglutide on the proliferation, migration, and osteogenic differentiation of human periodontal ligament cells

Pang

Yuan

Guo

et al. 2018

J of Periodontal Research

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Section: Discussionsupporting

confidence: 48%

The effect of liraglutide on the proliferation, migration, and osteogenic differentiation of human periodontal ligament cells

Pang

Yuan

Guo

et al. 2018

J of Periodontal Research

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“…This study's data support further investigation into the putative role(s) of Glp1r agonism in inflammatory, T-cellemediated diseases. Besides this observation, Glp1r agonism has already been proven to improve T-cellemediated murine disease models such as type 1 diabetes and experimental autoimmune encephalitis, 25,30,31 but clinical data are lacking. The anti-inflammatory effects of liraglutide described in this paper might also partly explain the improved surrogate renal endpoints observed in large randomized control trials in type 2 diabetes patients.…”

Section: Discussionmentioning

confidence: 99%

Glucagon-Like Peptide-1 Receptor Agonism Improves Nephrotoxic Serum Nephritis by Inhibiting T-Cell Proliferation

Filippidou

Kirsch

Thelen

et al. 2020

The American Journal of Pathology

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Glucagon-like peptide (GLP)-1 analogs such as liraglutide improved albuminuria in patients with type 2 diabetes in large randomized controlled trials. One of the suspected mechanisms is the antiinflammatory potential of GLP-1 receptor (Glp1r) agonism. Thus, the anti-inflammatory action of Glp1r agonism was tested in a nondiabetic, T-cellemediated murine model of nephrotoxic serum nephritis (NTS). The role of Glp1r in NTS was evaluated by using Glp1r À/À mice or C57BL/6 mice treated with liraglutide. In vitro, murine T cells were stimulated in the presence of liraglutide or vehicle. Glp1r À/À mice displayed increased renal infiltration of neutrophils and T cells after induction of NTS. Splenocyte proliferation and TH1 cytokine transcription were increased in spleen and lymph nodes of Glp1r À/À mice. Liraglutide treatment significantly improved the renal outcome of NTS in C57BL/6 mice by decreasing renal infiltration and proliferation of T cells, which resulted in decreased macrophage infiltration. In vitro, T cells stimulated in the presence of liraglutide showed decreased proliferation of TH1 and TH17 cells. Liraglutide blocked glycolysis in T cells and decreased their Glut1 mRNA expression. Together, Glp1r agonism protects mice from a T-celledependent glomerulonephritis model by inhibition of T-cell proliferation, possibly by interacting with their metabolic program. This mechanism may explain in part the renoprotective effects of Glp1r agonism in diabetic nephropathy.

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“…This notion requires further preclinical and clinical investigation to confirm the potential synergistic effect of these two therapeutic modalities. In addition, another GLP‐1R agonist, namely liraglutide, was found also to enhance the therapeutic effects of BM‐MSCs in type 1 DM 54 . Also, it was proved to improve glucose metabolism and decrease β‐cell apoptosis when co‐injected with UC‐MSCs 55 .…”

Section: Discussionmentioning

confidence: 99%

“…In addition, another GLP-1R agonist, namely liraglutide, was found also to enhance the therapeutic effects of BM-MSCs in type 1 DM. 54 Also, it was proved to improve glucose metabolism and decrease β-cell apoptosis when co-injected with UC-MSCs. 55 Interestingly, it was found to exert a bone protective effect in vivo through increasing OPG/RANKL ratio.…”

Section: Discussionmentioning

confidence: 99%

Exendin‐4 enhances osteogenic differentiation of adipose tissue mesenchymal stem cells through the receptor activator of nuclear factor‐kappa B and osteoprotegerin signaling pathway

Habib

Kamal

El-Maraghy

et al. 2022

J of Cellular Biochemistry

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The capability of mesenchymal stem cells (MSCs) to repair bone damage and defects has long been investigated. The receptor activator of nuclear factorkappa B (RANK), its ligand (RANKL) and the decoy receptor osteoprotegerin (OPG) axis is crucial to keep the equilibrium between osteoblastic and osteoclastic activity. Exendin-4 utilization increased bone formation and enhanced bone integrity. This study aimed to investigate the mentioned axis and determine the effect of exendin-4 upon adipose mesenchymal stem cells (Ad-MSCs) osteogenic differentiation. Ad-MSCs were isolated from rat epididymal fat, followed by characterization and then differentiation into osteocytes both in the presence or absence of exendin-4. Osteogenic differentiation was evaluated by alizarin red staining and the expression of osteogenic markers; using reverse transcriptase-quantitative polymerase chain reaction, western blotting and enzyme-linked immunoassay. MSCs derived from rat epididymal fat were isolated and characterized, along with their differentiation into osteocytes. The differentiated cells were alizarin redstained, showing increased staining intensity upon addition of exendin-4.Moreover, the addition of exendin-4 elevated the messenger RNA expression levels of osteogenic markers; runt-related transcription factor-2 (RUNX-2), osteocalcin, and forkhead box protein O-1 while reducing the expression of the adipogenic marker peroxisome-proliferator-activated receptor-gamma. Exendin-4 addition elevated OPG levels in the supernatant of osteogenic differentiated cells. Moreover, exendin-4 elevated the protein levels of glucagon-like peptide-1 receptor and RUNX-2, while decreasing both RANK and RANKL. In conclusion, osteogenic differentiation of Ad-MSCs is associated with increased osteoblastic rather than osteoclastic activity.

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Liraglutide Enhances the Efficacy of Human Mesenchymal Stem Cells in Preserving Islet ß-cell Function in Severe Non-obese Diabetic Mice

Cited by 9 publications

References 33 publications

The effect of liraglutide on the proliferation, migration, and osteogenic differentiation of human periodontal ligament cells

The effect of liraglutide on the proliferation, migration, and osteogenic differentiation of human periodontal ligament cells

Glucagon-Like Peptide-1 Receptor Agonism Improves Nephrotoxic Serum Nephritis by Inhibiting T-Cell Proliferation

Exendin‐4 enhances osteogenic differentiation of adipose tissue mesenchymal stem cells through the receptor activator of nuclear factor‐kappa B and osteoprotegerin signaling pathway

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