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© Uwe Maskos
Tranche d'hippocampe de souris colorée avec deux toxines spécifiques de sous-types de récepteur nicotinique, en rouge (grains), et en vert (corps cellulaires). L'hippocampe est la zone du cerveau qui gère la mémoire spatiale.
Publication : Physiology & behavior

Dimethyloxalylglycine preconditioning enhances protective effects of bone marrow-derived mesenchymal stem cells in Aβ- induced Alzheimer disease

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Physiology & behavior - 27 Nov 2018

Esmaeilzade B, Artimani T, Amiri I, Najafi R, Shahidi S, Sabec M, Farzadinia P, Zare M, Zahiri M, Soleimani Asl S

Link to Pubmed [PMID] – 30500334

Physiol. Behav. 2019 02;199:265-272

Mesenchymal stem cell (MSC) transplantation therapy has been proposed as a promising approach for the treatment of neurodegenerative disease. Chemical and pharmacological preconditioning before transplantation could optimize the therapeutic properties of transplanted MSCs. In this study, we hypothesized that preconditioning treatment with a prolyl hydroxylase inhibitor, dimethyloxalylglycine (DMOG), will increase MSC efficacy and paracrine effects in an amyloid-β (Aβ)-injected Alzheimer rat model. MSCs were incubated in different concentrations of DMOG for 24 h. Cell viability, migration, and antioxidant capacity was assessed in DMOG-treated and non-treated MSCs before transplantation into Aβ-injected rats. In vitro analysis revealed that DMOG treatment increased cell viability, migration, and expression of CXCR4, CCR2, Nrf2, and HIF-1α in the MSCs. Our in vivo results show that DMOG preconditioning enhances a MSC-mediated rescue of learning and memory function in Aβ-injected rats. Furthermore, we found an increased level of BDNF and total antioxidant capacity in the hippocampus of Aβ-injected rats following transplantation of preconditioned relative to untreated MSCs. Our results suggest that preconditioning MSCs with DMOG before transplantation may enhance the efficacy of stem cell based therapy in neurodegenerative disease.

https://www.ncbi.nlm.nih.gov/pubmed/30500334