SDF-1α/CXCR4-mediated migration of systemically transplanted bone marrow stromal cells towards ischemic brain lesion in a rat model

Wang, Ye; Deng, Yong; Zhou, Guangqian

doi:10.1016/j.brainres.2007.11.068

Cited by 257 publications

(195 citation statements)

References 37 publications

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“…Perrasso L. also showed that intravenous administration of BMSCs after global cerebral ischemia decreases hippocampal neural damage, suggesting that BMSCs increase neuron survival by intravenous infusion [3]. In our previous study, we demonstrated that EGFP-BMSCs migrate to hippocampus and cortex regions under ischemia condition after intravenous injection [36], indicating that BMSCs could pass blood-brain barrier and go to hippocampus and cortex. After transplantation into the body, MSCs have shown the ability to differentiate into neuron-like cells that secrete trophic factors such as VEGF [32], BDNF [8], and NGF [37], which play important roles in protecting the injured neurons.…”

Section: Discussionmentioning

confidence: 85%

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Hypoxia-Inducible Factor 1-α-AA-Modified Bone Marrow Stem Cells Protect PC12 Cells from Hypoxia-Induced Apoptosis, Partially Through VEGF/PI3K/Akt/FoxO1 Pathway

Zhong

Zhou

et al. 2012

Stem Cells and Development

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Section: Discussionmentioning

confidence: 85%

“…area attracts BMSCs to the ischemic lesion of brain [36]. EPO has been shown to get rid of ROS and have anti-inflammation effects in ischemia brain [38].…”

mentioning

confidence: 99%

Hypoxia-Inducible Factor 1-α-AA-Modified Bone Marrow Stem Cells Protect PC12 Cells from Hypoxia-Induced Apoptosis, Partially Through VEGF/PI3K/Akt/FoxO1 Pathway

Zhong

Zhou

et al. 2012

Stem Cells and Development

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“…Almost all of these studies have shown upregulation of CXCL12, in some form, in and around the site of injury. Some examples of injury include skin burns Xu et al, 2013;Yang et al, 2013), brain lesions (Wang et al, 2008b) and skeletal fracture injury (Kitaori et al, 2009). In one of these studies, CXCL12 production reached peak levels at day 7 post injury (Hu et al), whilst in another, the chemokine displayed bimodal upregulation, with levels peaking at day 1 and then again at day 5 post wounding .…”

Section: Mechanisms Of Msc and Pericyte Recruitment To Sites Of Injurymentioning

confidence: 99%

Pericytes, mesenchymal stem cells and their contributions to tissue repair

Wong

Rowley

Redpath

et al. 2015

Pharmacology & Therapeutics

152

110

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Regenerative medicine using mesenchymal stem cells for the purposes of tissue repair has garnered considerable public attention due to the potential of returning tissues and organs to a normal, healthy state after injury or damage has occurred. To achieve this, progenitor cells such as pericytes and bone marrow-derived mesenchymal stem cells can be delivered exogenously, mobilised and recruited from within the body or transplanted in the form organs and tissues grown in the laboratory from stem cells. In this review, we summarise the recent evidence supporting the use of endogenously mobilised stem cell populations to enhance tissue repair along with the use of mesenchymal stem cells and pericytes in the development of engineered tissues. Finally, we conclude with an overview of currently available therapeutic options to manipulate endogenous stem cells to promote tissue repair.

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“…The activation of the CXCR4/SDF-1α signaling pathway on NPCs and MSCs increases their migratory capacity, survival, and remyelinating capacity, both in vitro on slice cultures (Corti et al, 2005;Imitola et al, 2004b), as well as in vivo upon focal transplantation into rodents with experimental cerebral ischemia (Robin et al, 2006;Wang et al, 2008), and JHMV-induced demyelination (Carbajal et al, 2010(Carbajal et al, , 2011. In human NPCs, integrins α2, α6, and β preferentially mediate the homing toward the vasculature, whereas the CXCR4/ SDF-1α signaling pathway regulates homing through the brain parenchyma (Carbajal et al, 2010;Mueller et al, 2006;van der Meulen et al, 2009).…”

Section: Homing and Extravasationmentioning

confidence: 99%

How stem cells speak with host immune cells in inflammatory brain diseases

Pluchino

Cossetti

2013

Glia

111

109

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Advances in stem cell biology have raised great expectations that diseases and injuries of the central nervous system (CNS) may be ameliorated by the development of non-hematopoietic stem cell medicines. Yet, the application of adult stem cells as CNS therapeutics is challenging and the interpretation of some of the outcomes ambiguous. In fact, the initial idea that stem cell transplants work only via structural cell replacement has been challenged by the observation of consistent cellular signaling between the graft and the host. Cellular signaling is the foundation of coordinated actions and flexible responses, and arises via networks of exchanging and interacting molecules that transmit patterns of information between cells. Sustained stem cell graft-to-host communication leads to remarkable trophic effects on endogenous brain cells and beneficial modulatory actions on innate and adaptive immune responses in vivo, ultimately promoting the healing of the injured CNS. Among a number of adult stem cell types, mesenchymal stem cells (MSCs) and neural stem/precursor cells (NPCs) are being extensively investigated for their ability to signal to the immune system upon transplantation in experimental CNS diseases. Here, we focus on the main cellular signaling pathways that grafted MSCs and NPCs use to establish a therapeutically relevant cross talk with host immune cells, while examining the role of inflammation in regulating some of the bidirectionality of these communications. We propose that the identification of the players involved in stem cell signaling might contribute to the development of innovative, high clinical impact therapeutics for inflammatory CNS diseases.

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SDF-1α/CXCR4-mediated migration of systemically transplanted bone marrow stromal cells towards ischemic brain lesion in a rat model

Cited by 257 publications

References 37 publications

Hypoxia-Inducible Factor 1-α-AA-Modified Bone Marrow Stem Cells Protect PC12 Cells from Hypoxia-Induced Apoptosis, Partially Through VEGF/PI3K/Akt/FoxO1 Pathway

Hypoxia-Inducible Factor 1-α-AA-Modified Bone Marrow Stem Cells Protect PC12 Cells from Hypoxia-Induced Apoptosis, Partially Through VEGF/PI3K/Akt/FoxO1 Pathway

Pericytes, mesenchymal stem cells and their contributions to tissue repair

How stem cells speak with host immune cells in inflammatory brain diseases

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