All‐trans retinoic acid preconditioning enhances proliferation, angiogenesis and migration of mesenchymal stem cell <i>in vitro</i> and enhances wound repair <i>in vivo</i>

Pourjafar, Mona; Saidijam, Massoud; Mansouri, Kamran; Ghasemibasir, Hamid Reza; Dermani, Fateme Karimi; Najafi, Rezvan

doi:10.1111/cpr.12315

Cited by 73 publications

(63 citation statements)

References 58 publications

(98 reference statements)

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“…However, low migration, survival, and neural differentiation rates are the key factors in determining therapeutic efficacy in translational studies (Chakari-Khiavi et al, 2019). Accumulating evidence has demonstrated that the preconditioning of stem cells prior to transplantation could promote cell survival and efficacy (Pourjafar et al, 2017;Hu and Li, 2018;Esmaeilzade et al, 2019). Resveratrol, an activator of SIRT1, is an antiaging regent which could protect cells against oxidative stress and nutrient stressors FIGURE 5 | MSCs and RES-MSCs regulated the expression of APP in mouse hippocampus.…”

Section: Discussionmentioning

confidence: 99%

RETRACTED: Resveratrol Preincubation Enhances the Therapeutic Efficacy of hUC-MSCs by Improving Cell Migration and Modulating Neuroinflammation Mediated by MAPK Signaling in a Mouse Model of Alzheimer’s Disease

Wang

et al. 2020

Front. Cell. Neurosci.

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Human umbilical cord-derived mesenchymal stem cells (hUC-MSCs) are promising for the treatment of Alzheimer's disease (AD). However, their low rate of migration and survival in the brain limit their clinical applicability. This study is designed to improve the therapeutic potential of hUC-MSCs by preincubating them with resveratrol, a natural polyphenol capable of regulating cell destiny. Herein, we demonstrate that resveratrol preincubation enhances the migration of hUC-MSCs in vitro, as well as their survival and homing into the hippocampus of AD mice in vivo. Moreover, resveratrol-primed MSCs were better able to inhibit amyloid-β peptide (Aβ) deposition, Tau hyperphosphorylation, and oxidative stress, all while improving learning and memory. Notably, we found that hUC-MSCs inhibited neuroinflammation by reacting with astrocytes and microglial cells and suppressing mitogen-activated protein kinases (MAPKs), extracellular signal kinases (ERK), p38 kinases (p38), and c-Jun N-terminal kinases (JNK) signaling pathways in the hippocampus of AD mice. Furthermore, resveratrol pretreatment enhanced these effects. Conclusively, the current study revealed that resveratrol preconditioning protected hUC-MSCs against the hostile microenvironment characteristic of AD and enhanced their viability and homing into the brain of AD mice. The use of resveratrol-pretreated hUC-MSCs is thereby proposed to be a promising therapy for AD.

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Section: Discussionmentioning

confidence: 99%

RETRACTED: Resveratrol Preincubation Enhances the Therapeutic Efficacy of hUC-MSCs by Improving Cell Migration and Modulating Neuroinflammation Mediated by MAPK Signaling in a Mouse Model of Alzheimer’s Disease

Wang

et al. 2020

Front. Cell. Neurosci.

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“…The treatment of MSCs with deferoxamine (DFO), cobalt chloride, or hydralazine can lead to increased surface expression of HIF-1a proteins, resulting in transcription of genes involved in cell migration [81][82][83][84] . In addition, pretreatment with all-trans retinoic acid [85] , melatonin [86] , estrogen receptorα (ERα) [87] , and certain extracts from traditional Chinese herbs (i.e. Polydatin [88] and Exenatide [89] ) can enhance the migration of MSCs as well [90] .…”

Section: Pretreatment Of Mscs With Cytokines and Small Moleculesmentioning

confidence: 99%

Strategies to improve the migration of mesenchymal stromal cells in cell therapy

Chen

et al. 2017

Transl. Neurosci. Clin.

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KEYWORDSMSCs; migration; cell therapy; engraftment efficiency; neurological disorder Mesenchymal stromal/stem cells (MSCs) are multipotent cells under consideration as a potential new therapy for a variety of inflammatory diseases including certain neurological disorders. It is generally thought that the efficacy of cell therapy in attenuating damage after ischemia, inflammation, or injury depends on the quantity of transplanted cells recruited to the target tissue. However, only a small number of systematically infused MSCs can effectively migrate to target sites, which significantly decreases the efficacy of exogenous cell-based therapy. In this review, we discuss specific factors influencing MSC migration, and summarize current strategies that effectively promote the motility of MSCs. In addition, we describe several protocols to improve the migration of stromal cells into the nervous system and, therefore, enhance the efficiency of engraftment as means of treating neurological disorders.Citation Li G, Hu Y, Chen Y, Tang Z. Strategies to improve the migration of mesenchymal stromal cells in cell therapy. Transl. Neurosci. Clin. 2017, 3(3): 159-175.

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“…Hypoxic condition is intricately involved in angiogenesis, osteogenesis, and bone regeneration and remodelling, and hypoxia‐inducible factor 1α (HIF‐1α) is the master transcriptional regulator of osteogenic‐angiogenic coupling under hypoxia . Physiological hypoxic stress has a major role in bone defect regeneration in regulating cell mobility and angiogenesis . Unfortunately, acute severe hypoxia significantly endangers the cell mobility of BMSCs, but little is known about the effect of severe hypoxia on cell adhesion capacity and proangiogenic capacity of BMSCs.…”

Section: Introductionmentioning

confidence: 99%

“…8,9 Physiological hypoxic stress has a major role in bone defect regeneration in regulating cell mobility 10,11 and angiogenesis. 12 Unfortunately, acute severe hypoxia significantly endangers the cell mobility of BMSCs, 13 but little is known about the effect of severe hypoxia on cell adhesion capacity and proangiogenic capacity of BMSCs. Protecting BMSCs from the severe hypoxiainduced negative effects on the cell behaviour at the initial stage after transplantation may play a key role for followed tissue repair.…”

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confidence: 99%

ERK1/2 and Akt phosphorylation were essential for MGF E peptide regulating cell morphology and mobility but not proangiogenic capacity of BMSCs under severe hypoxia

Sha

Yang

2018

Cell Biochemistry & Function

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Sever hypoxia impairs bone defect repair with bone marrow-derived mesenchymal stem cells (BMSCs). This study proved that mechano-growth factor E (MGF E) peptide could improve the severe hypoxia-induced cell contraction and decline of cell adhesion and migration of BMSCs. Besides, MGF E peptide weakened the effects of severe hypoxia on the cytoskeleton arrangement- and mobility-relevant protein expression levels in BMSCs. The underlying molecular mechanism was also verified. Finally, it was confirmed that MGF E peptide showed an adverse effect on the expression level of vascular endothelial growth factor α in BMSCs under severe hypoxia but could make up for this deficiency through accelerating cell proliferation.

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All‐trans retinoic acid preconditioning enhances proliferation, angiogenesis and migration of mesenchymal stem cell in vitro and enhances wound repair in vivo

Abstract: Pre-conditioning of MSCs with ATRA increased efficacy of cell therapy by activation of survival signalling pathways, trophic factors and release of pro-angiogenic molecules.

Cited by 73 publications

References 58 publications

RETRACTED: Resveratrol Preincubation Enhances the Therapeutic Efficacy of hUC-MSCs by Improving Cell Migration and Modulating Neuroinflammation Mediated by MAPK Signaling in a Mouse Model of Alzheimer’s Disease

RETRACTED: Resveratrol Preincubation Enhances the Therapeutic Efficacy of hUC-MSCs by Improving Cell Migration and Modulating Neuroinflammation Mediated by MAPK Signaling in a Mouse Model of Alzheimer’s Disease

Strategies to improve the migration of mesenchymal stromal cells in cell therapy

ERK1/2 and Akt phosphorylation were essential for MGF E peptide regulating cell morphology and mobility but not proangiogenic capacity of BMSCs under severe hypoxia

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